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A Text Book of Veterinary Pathology 



A TEXT BOOK 



OF 



VETERINARY 
PATHOLOGY 



FOR 



STUDENTS AND PRACTITIONERS 



BY 

A. T. KINSLEY, M. Sc, D. V. S. 

Pathologist, Kansas City Veterinary College 



FULLY ILLUSTRATED 



CHICAGO 

ALEXANDER EGER 

1910 



/A L 



n 






\ 



0< 



Copyrighted at Washington, D. C, by 

ALEXANDER EGER 

1910 



CI.A2?1281 



LINDEN BROS. PF.CSS, CHICAGO 



* " ' PREFACE. 



A knowledge of pathology is essential to practitioners and 
to students of medicine. The general considerations of pathol- 
ogy, whether in reference to diseases of the human or diseases 
of domestic animals, are practically identical. Many textbooks 
on this subject are available, but they are especially written for 
the practitioner and student of human medicine, and the illus- 
trations and examples are all in reference to diseases of the 
human. Such textbooks have been used by the author for sev- 
eral years in veterinary classes and it was thought that if the 
same general pathological principles could be exemplified by 
cases and illustrations in veterinary medicine, the subject mat- 
ter would be more readily understood by the veterinarj^ student. 
This explains the issuance of the present volume. 

The writer has endeavored to place every phase of pathol- 
ogy from the veterinarian's point of view. The entire subject 
matter has been expressed as far as possible in common every- 
day language, with the hope that all readers will have no trou- 
ble in grasping the pathologic facts. An extensive glossary has 
been appended and will be of considerable aid because practi- 
cally every technical term, with its analysis and definition, will 
be found therein. 

The author is greatly indebted to Dr. S. Stewart, Dean of 
the Kansas City Veterinary College ; Dr. D. M. Campbell, edi- 
tor of The American Journal of Veterinary Medicine ; Prof. W. 
E. King, Bacteriologist of the Kansas State Agricultural College; 
Dr. F. J. Hall, Chief of the Food Inspection Department Kan- 
sas City, Mo., and formerly pathologist of the ]\Iedical Depart- 
ment University of Kansas ; Dr. L. Rosenwald, formerly patholo- 
gist of the Kansas City Veterinary College ; Dr. Geo. F. Babb, 
Milk Inspector of the city of Topeka, Kansas; Dr. D'. Cham- 
plain, editor of The Milk-Man, for suggestions made by them 
concerning the text matter. Also Dr. R. F. Bourne, physiologist 
of the Kansas City Veterinary College ; Dr. C. D. Folse, City 
]\Iilk and Meat Inspector of Marshall, Texas, and Mr. Chas. Sals- 
bery, microscopic laboratory assistant in the Kansas City Vet- 
erinarv College, for their assistance in the preparation of the 
illustrations. 

The author consulted various text-books, journals and other 
publications while preparing the text for which acknowledge- 
ment is hereby made. 

If this book supplies the practitioner and the student of 
veterinary medicine with clear, concise statements of veterinary 
pathology, the purpose of the book has been fulfilled. 

A. T. K. 



CONTENTS. 

PAGE 

Preface 5 

CHAPTER I. 

Definitions 19 

The Cell 20 

CHAPTER H. 

General Consideration of Disease 34 

Table of Vegetable Parasites 48 

Saccharomyces . 51 

Schizomycetes 52 

Animal Parasites 62 

Protozoa _ 63 

Helminthes 63 

Arthropoda 69 

CHAPTER HL 

Immunity 78 

CHAPTER IV. 

Malformations 92 

CHAPTER V. 

Circulatory Disturbances 110 

Hemorrhage 112 

Lymphorrhagia 117 

Oedema, Dropsy or Hydrops 118 

Thrombosis 122 

Embolism ,....-. 128 

Ischemia •pc.^t^ • ^^- r 1^2 

\^ Hyperemia (Passive) 133 

Hyperemia (Active) 135 

CHAPTER VL 

Inflammation 138 

CHAPTER VII. 

Progressive Tissue Changes 177 

Regeneration 177 

i 



11 CONTENTS. 

PAGE 

Wound Healing 183 

Hypertrophy 188 

Hyperplasia 191 

Metaplasia . . . , 193 

CHAPTER VIII. 

Retrogressive Tissue Changes 195 

Atrophy 196 

Cloudy Swelling • • • • • ^00 

Fatty Changes 203 

Amyloid Changes 210 

Hyaline Changes ...... 212 

Mucoid Changes 214 

Colloid Changes 217 

Serous Infiltration 220 

Glycogenic Infiltration 221 

Uratic Infiltration 223 

Keratosis 224 

Ossification , 226 

Calcareous Infiltration 227 

Calculi 230 

Concrements 238 

Pigmentary Changes 241 

Excessive Pigmentation 243 

Absence of, or Diminished Pigmentation 249 

CHAPTER IX. 

Necrosis and Death 251-262 

Physiologic Death 262 

Pathologic Death 263 

CHAPTER X. 

Tumors 267 

Fibroma 278 

Mixoma ' 282 

Chondroma 283 

Osteoma 288 

Glioma 289 

Odontoma 289 

Neiu-oma 293 

Angioma 293 

Myoma 296 

Sarcoma 298 



CONTENTS. Ill 

Papilloma 318 

Embryonic Epithelial Tumors 321 

Placentoma 331 

Teratoma 332 

Cysts . 335 

CHAPTER XL 

Fever 339 

CHAPTER Xn. 

Infective Granulomata 344 

Tuberculosis 344 

Actinomycosis 345 

Glanders 361 

Epitheloma Contagiosum 371 

Glossary 373 



LIST OF INSERTS. 

Insert I — Botanical Names Next to page 45 

Insert II — Bacteria Next to page 62 

Insert III — ^Protozoa Next to page 63 

Insert IV — Helminthes Next to page GQ 

Insert V — Arthropoda Next to page 71 

Table I — Table of Tumors Next to page 335 



A LIST OF THE ILLUSTRATIONS. 

FIGURE Page 

I — Diagram of a Typical Cell 21 

2.^ 3 — Amitosis 25 

4 — Division oi Nucleus 26 

5 — Division of Cell 26 

6— Cell in Resting Stage 27 

7 — Prophase, Showing Division of Centrosome 27 

8 — Prophase, Showing Separation of Centrosomes • • 27 

9 — Metaphase 27 

10, 1I4 12, 13 — Indirect Cell Division — Metaphase, Anaphase, Telophase 28 

14 — Ciliated Epithelium, Trachea 29 

15 — Spermatozoa 30 

16 — Red Buckeye 46 

17 — Astragalus Molissimus 47 

18 — Trichophyton Tonsurans • 49 

19 — Aspergillus Fumigatus 50 

20 — Saccharomyces Farciminosus Si 

21 — Group Bacteria 53 

22, 23 — ^Group Bacteria 53 

24 — Flagellate Bacteria 54 

25 — Capsulated Bacteria 54 

26 — Bacterial Fission 56 

27 — Sporulation 57 

28 — Bacillus Anthracis 59 

29 — Bacillus Tetani 60 

30 — Piroplasma Bigeminum (i2 

31 — Trypanosoma Evansi (From Kaupp Parasites) ^z 

32 — Sarcocystis Miescheri (From Kaupp Parasites) 64 

ZZ — Taenia Marginata 65 

34 — Taenia Canina ^ 

35 — Taenia Echinococcus 66 

2,^ — Taenia Solium (ij 

2>7 — Strongylus Micrurus 6y 

38 — Strongylus Paradoxus 68 

39 — Filaria Papillosa 68 

40 — Oxyuris Curvula 69 

41 — 'Syngamus Trachealis 70 

42 — Sclerostoma Hypostomum 70 

43 — Trichocephalus Depressiusculus 70 

44 — Melophagus Ovinus 71 

iv 



FI6URE PAGE 

45 — Gastrophilus Equi 72 

46 — Oestrus Ovis 72 

47 — Culex Pungens Tz 

48 — A^caris Mystax * 74 

49 — Dlstoma Hepaticum 74 

50 — Echinorhynchus Gigas 75 

51 — Trichina Spiralis 76 

52 — Trichodectes Latus ']6 

53 — Hematopinus Phalanges Ovis 79 

54 — Pulex Serraticeps 79 

55' — Margarapus Annulatus, Female 80 

56 — Margarapus Annulatus, Male 80 

57 — Margarapus Annulatus, Female laying eggs 80 

58 — Margarapus Annulatus Larva 80 

59 — Ixodes Ricinus 81 

60 — Psoroptes Communis Ovis 82 

61 — Demodex Folliculorum Canis (From Kaupp Parasites) 83 

62. — Immunity, Bacterial 85 

^Z — Hematoba Serrata 86 

64 — Immunity, Toxin 86 

65 — Uncinaria Canina .,. . . 88 

(^ — Cranio, Schisis 95 

^7 — Chelio, Schisis 96 

^ — Palato, Schisis 97 

69 — Abdomino, Schisis 97 

70 — Synophthalmia 98 

71 — Solipedia 99 

72 — Polydactilism 100 

72) — Prognathism lOi 

74 — Schistosis, Melus xA.nticus 102 

75 — Ectocardia 104 

76— Dicephalic, Calf 108 

77 — Dicephalic, Calf 108 

78 — Petechial Hemorrhage 113 

79 — Hematoma 114 

80 — Ascites, Dog 119 

81 — Subcutaneous Oedema, Horse 120 

82 — Thrombus in Vessels 125 

^Z — Thrombus, Red 126 

84 — Embolism 129 

85 — Infarction, Spleen 130 

86 — Hyperaemia Hemorrhage and Oedema Intestine 135 

87 — Hyperaemia Kidney 136 

88, 89, 90, 91— Vascular Variations in Inflammation 147- 148- 149- 150 

92 — Types of Cells in Inflammatory Exudates 151 

93 — 'Gastritis 153 

94 — Acute Pleurisy 154 



VI LIST OF ILLUSTRATIONS. 

FIGURE PAGE 

95 — Acute Meningitis 156 

96 — Grey Hepatization 157 

97 — Fibrinous Pleurisy 158 

98 — Myositis,. Acute 160 

99 — Chronic Pneumonia 162 

100 — Chronic Hepatitis 165 

loi — Pus, from a case of Strangles 168 

102 — Suppurative Nephritis 170 

103 — Red Hepatization 172 

104 — Vascular Regeneration 178 

105 — Fibrous Regeneration 179 

106 — Wound Healing 185 

107 — Exuberant Granulation 187 

108 — Hyperplasia Interstitial Testicular Cells 191 

109 — Hyperplasia Ureter 192 

1 10 — Metaplasia 194 

1 1 1 — Cloudy Swelling 201 

112 — Fatty Infiltration, Liver 206 

113 — Fatty Degeneration, Liver 209 

114 — Amyloid Degeneration, Liver 212 

IIS — HyaHne Degeneration, Vessels 213 

116 — Mucoid Degeneration 216 

117 — Colloid Degeneration 218 

118 — Colloid Degeneration 219 

1 19 — Keratotic Growth 225 

120 — Atheromatus Degeneration 229 

121 — Group Calculi 230 

122 — Vesicular Calculi 233 

123 — Preputial and Renal Pelvic Calculi 234 

124 — Salivary Calculi 235 

125 — Intestinal Calculus 236 

126 — Biliary Calculi 237 

127 — Hair Balls 239 

128 — Inspissated Pus 240 

129 — Hemosidern Pigmentation 244 

130 — Icteric Pigmentation 246 

131 — Necrosis 253 

132 — Bacillus Necrophorus 254 

133— Ergot 255, 

134 — Ergot Poisoning Cattle 256 

135 — Fatty Necrosis 258 

T36 — Necrotic Center of Tubercle 259 

137 — Sarcoma 270 

138 — Metastatic Sarcomata 273 

139 — Epithelioma, Horse Head 275 

140 — Hard Fibroma 279 

141 — ^Soft Fibroma 280 



LIST OF ILLUSTR.\TIONS. Vll 

FtGUBE PACK 

142 — Myxoma 282 

143 — Chondroma 284 

144 — Lipoma, Horse 286 

145 — Lipoma, Ox 287 

146 — Osseous Tumor, Maxilla 288 

147 — Odontoma, Horse 290 

148 — Odontoma, Epithelial ' 292 

149 — Hemangioma, Simplex 294 

150 — Hemangioma Cavernosum 295 

151 — Hemangioma Hypertrophicum ' 296 

152 — Leiomyoma, Small Intestine 297 

153— Leiomyoma, Microscopic 298 

154 — Sarcoma, Horse ^ 299 

155 — Sarcoma Mediastinum (Sections of Tumor) 300 

156 — tSarcoma, Round Cell , 301 

157 — Lympho-Sarcoma Heart 302 

158 — Lympho-Sarcoma 303 

159 — Spindle Cell Sarcoma, Mule 304 

160 — Spindle Cell Sarcoma 305 

161 — Myeloid or Giant Cell Sarcoma 306 

162 — Mixed Cell Sarcoma, Horse 307 

163 — Mixed Cell Sarcoma, Jaw 308 

164 — Mixed Cell Sarcoma 309 

165 — Alveolar Sarcoma 310 

166 — Endothelioma 311 

167 — Endothelioma 312 

168 — Uterine Sarcoma 313 

169 — Melano-Sarcoma, Horse 314 

170 — Melano-Sarcoma, Hog Skin 315 

171 — Melano-Sarcoma, Microscopic, of Horse's Liver 316 

172 — Myxo-Sarcoma 317 

173 — Papillomatosis, Horse 319 

174 — Papilloma, Microscopic 320 

175 — Carcinoma 322 

176 — Epithelioma, Microscopic 323 

177 — Epithelioma, Microscopic 324 

178 — Epithelioma, Pearl Cell 325 

179 — Adenoma, Mammae 326 

180 — Adenoma, Microscopic 327 

181 — Adeno-Sarcoma, Microscopic 328 

182 — Cystadenoma 329 

183 — Hypernephroma 330 

184 — Dermoid Cyst 332 

185 — Dermoid Cyst, Eye ;^^;^ 

186 — Dentigerous Cyst 334 

187 — Cyst, Dog Neck ;^;^6 

188 — Uterine Cyst ^ ^;^y 



Vlll LIST OF ILLUSTRATIONS. 



FIGURE 



PAGE 

189 — Fever — Crisis and Lysis 340 

190 — Continuous Fever 342 

191 — Remittent Fever, Curve 342 

192 — Intermittent Fever, Curve 343 

193 — Bacterium Tuberculosis, Bovine 345 

194 — Small Cellular Tubercular Liver 348 

195 — Tuberculosis Lesion Later 350 

196 — Tuberculosis Mammary Gland 351 

197 — Ray Fungus (Actinomyces) 356 

198 — Actinomycotic Tongue 359 

199 — Bacillus Mallei 362 

2G0 — Glanders Lesion, Farcy 365 

201 — Glanders, Nasal Ulcer ^6^ 

202 — Glanders, Microscopic 357 

203 — Epithelioma, Contagiosum , 369 

204 — Epithelioma, Contagiosum 370 

205— Epithelioma, Contagiosum, Microscopic 371 



CHAPTER I. 
DEFINITIONS. 

Pathology is the science of disease. It is the science which 
treats of the nature, causes, progress, symptoms and termina- 
tion or result of disease. It includes etiology, i. e., the study 
of the causes of disease, and pathogenesis, that is, the study of 
the course, abnormal functions and lesions produced in disease. 

General Pathology is confined to the explanation of the sum- 
mary of the facts obtained in the study of special pathology. It 
is concerned essentially in the solution of general principles of 
those morbid conditions that are common to the entire organism, 
as malformation, degeneration, regeneration, inflammation, neo- 
•formation and fever. 

Special Pathology deals with all the abnormalities or diseased 
conditions of one part or organ as the diseases of the ear, skin, 
etc., and consequently special pathology is further subdivided 
into otologic pathology, dermatologic pathology, etc. 

Pathologic Physiology, is that part of pathology which has to 
do with the investigation and description of abnormal functions 
of a diseased organ or animal. The pathologic physiology is, 
in many cases7 the principle symptom of a disease, e. g., paraly- 
sis of the radial nerve. Abnormal function is frequently the 
only evidence discernible in a disease, e. g., epilepsy. 

Pathologic Anatomy, or morbid anatomy, is concerned in the 
structural changes in a diseased tissue or organ. Pathologic 
changes in the structure of a tissue or organ are collectively 
termed lesions. Lesions may be sufficiently gross that they are 
readily observed with the unaided eye or thev may be so min- 
ute that the miscroscope is necessary for their detection. The 
investigation and the recording of facts observed in the study 
of gross and minute lesions are included in gross, or macroscopic 
pathologic anatomy and minute, or microscopic pathologic an- 
atomy respectively. 

Human Pathology has to do with the facts observed in the 
study of the diseases of the human. 

Comparative Pathology, is the name applied to the study of 
the diseases of all animals in which the diseases of one genus, 
(group of animals) is taken as a standard and the diseases of all 
other animals are discussed in comparison with the type selected. 

Veterinary Pathology, is a discourse on the diseases of domestic 
animals. 

19 



20 VETERIN.ARY PATHOLOGY. 

THE CELL. 

ANATOMIC. 
Structure. 

Body. 

Nucleus. 

Centrosome. 

Membrane. 
Shape. 
Size 
PHYSIOLOGIC. 
Growth. 
Reproduction. 
Motion. 
Metabolism. 

AnaboUsm. 

Katabolism. 
IRRITABILITY. 

Structurally, an animal body is composed of definitely ar- 
ranged parts, called organs. An organ is a portion of the body 
having a particular function and is, structurally, a tissue-complex 
in which each tissue has a certain definite proportion and relation. 
A tissue is composed of like or similar cells with more or less 
inter' llular substance interposed. The intercellular substance is 
usual / a product of the cells. A cell has been defined as a 
microscopic mass of protoplasm containing sufficient individ- 
uality to possess a life history. 

The function of an animal body is the sum total of the corre- 
lated functions of its component tissues. The function of a 
tissue is the sum total of the function of its cells. Thus a cell 
represents the anatomical or structural unit and the physiologic 
or functional unit of all animal bodies. 

In ancient times disease was thought to be the result of 
the entrance into the body of some "evil spirit," and the symp- 
toms presented during disease was evidence of the struggle 
beween the body and the *'evil spirit." During the middle ages, 
Hippocrates, "The Father of Medicine," established the Hippo- 
cratic Theory of disease. Hippocrates taught, 1st, that the body 
was composed of four humors, viz., blood, phlegm, yellow bile 
and black bile ; 2nd, that health consisted of the proper balance 
of the humors ; and 3d, that disturbed proportions of the hum- 
ors resulted in disease. 

Modern pathology is based upon the knowledge of cell activi- 
ties. Virchow was the father of cellular pathology. He first 
taught the cellular theory to students of pathology and he first 
advocated it in published articles. Cellular physiology was really 
an outgrowth of cellular pathology. A knowledge of cells is 



THE CELL. 



21 



indispensable in the study of pathology and a brief description 
is here appended. 

Structure — Cells are variable in structure. The active consti- 
tuent of all animal cells is protoplasmic in nature. The essen' 
tial parts of animal cells are the cell-body, nucleus and centro- 
some. 

The cell-body is present in pratically all cells. It is com- 
posed of semisolid protoplasm, a portion of which is of a stringy 



13-- 
« — 

It -- 

10- 




Fig. 1 — Diagi-am of a Typical Cell, after Bohm-Davidoff-Hubpr. 



1. Vaxuoles. 

2. Cell-membrane. 

3. Exoplasm. 

4. Nuclear membrane. 

5. Nucleolus. 

6. Chromatin net-knot. 

7. Centrospbere. 



8. Centrosome. 

9. Foreign inclosures. 

10. Hyaloplasm. 

11. Spongioplasm. 

12. Chromatin network. 

13. Linin network. 

14. Nucleoplasm. 



consistency and is termed spongioplasm. In the meshes of the 
spongioplasm there is found a fluid protoplasm, designated hya- 
loplasm. The relative proportion of spongioplasm and hyalo- 



22 VETERINARY PATHOLOGY. 

plasm varies in different cells and even in different parts of 
tli^ same cell. Particles of food and various other insoluble sub- 
stances are not uncommon in the cell body. Vacuoles are fre- 
quently observed, especially in wandering cells. 

The nucleus is constant in all functioning or active cells except 
the mammalian red blood corpuscles, and some of the pulmonary 
alveolar epithelial cells. The nucleus appears as a dense body 
and is usually centrally located in the cell body. The relative 
proportion of nucleus to cell body is inconstant, e. g., the 
lymphocyte is practically all nucleus ; some epithelial cells have 
a very small nucleus and a very large cell body. The nucleus 
varies in shape from a sphere to an irregular mass, and is sur- 
rounded by an incomplete membrane. The essential structure 
of the nucleus is a chromatin network. The spongioplasm 
and hyaloplasm of the cell body are continuous through the 
incomplete nuclear membrane into the nucleus where they are 
designated linin and nucleoplasm respectively. The nucleus may 
also contain a nucleolus which is probably a knot in the chro- 
matin network. 

The centrosome is a dense refractile body found in the 
nucleus or in the cell body just outside the nuclear membrane. 
Many fine radiating fibres may extend outward from the centro- 
some. 

A cell membrane may or may not be present. This mem- 
brane is formed by a condensation of the substance of the cell 
body. The sarcolemma of a muscle fibre is perhaps the most 
typical cell membrane found in animal cells, the red corpuscle 
has a modified cell membrane. A nerve cell possesses a neuri- 
lemma, although it is probably not a true cell membrane. 

Shape. — Embryonic cells are usually spherical in shape and 
it is probable that sphericity is a primitive quality of cells. The 
shape of matured cells is determined by their function and loca- 
tion. External surface cells are usually flat and when subject 
to pressure and friction they are arranged in strata, i. e., they 
are stratified. The cells lining the air vesicles are flat because 
of the necessity of the exchange of gases through them. Muscle 
cells are elongated to allow of contraction to produce motion. 
Goblet cells are large and more or less spherical because of the 
elaboration of mucus in them. Accommodation to space pro- 
duces variation in the shape of cells, thus ; fat cells are originally 
spherical, but because of pressure, they become polyhedral. Cells 
vary from the flat pavemental cells to those spherical in shape. 

Pressure is probably the most important factor in the produc- 



THE CELL. 23 

tion of pathologic variation in cell morphology. Thus parenchym- 
atous cells, as hepatic and renal cells, frequently become com- 
pressed by hyperplastic interstitial tissue sufficiently to change 
their shape from polygonal or cuboidal to irregularly flattened or 
fusiform. Columns of tumor cells may become pressed suffi- 
ciently by the invaded tissue to produce scale like cells or the so- 
called pearl cells. On the other hand, the same variety of tumor 
cells developed in tissue in which mutual pressure is limited, 
assume sphericity. 

Size. — Cells vary in size from the lymphoid cells that are 
from 4 to 8 microns in diameter to the marrow cells that are 
from 30 to 60 microns in diameter. The size of the cell is 
characteristic of the tissue they compose. Equalization of the 
surface and mass is a factor in the determination of the size of 
cells. Function of cells also has some bearing upon their size; 
thus, cells that have the power of independent motion and rap- 
idly acting cells are usually small. Fpod is no doubt a deter- 
mining factor in the size of cells. Ova are large because of the 
storage of food. 

Pathologic variation in the size of cells is of common occur- 
rence. Hypertrophy is the abnormal enlargement of individual 
cells. The size of red blood cells is variable in pernicious ane- 
mia, (swamp fever), of the horse. Several cells may fuse, 
forming a cell-complex, syncytium, or giant cell in and arouna 
foreign bodies, and in tubercular and actinomycotic lesions. 

Growth. — Growth in cells is the exercise of that property or 
function which results in their enlargement or it is the process 
by which they are increased in size. That cells do grow is self- 
evident and is common knowledge. A central, polymeric pro- 
tein-molecule is supposed to be the essential structure of all 
active cells. This central, polymeric molecule is probably unsat- 
urated and new simple molecules may be serially combined 
with it and then the cell becomes larger and grows. This prop- 
erty of cells is especially evident during the embryonic period 
but gradually diminishes to the time of maturity, when it is 
largely supplanted by other functions. The growth of cells is 
accompanied by the accummulation of energy. The larger a 
cell, other things being equal, the greater the potential energv. 
All functioning of cells, except growth, is accompanied by the 
liberation of energy. Growth results in accummulation of poten- 
tial energy and other functions convert potential into kinetic 
energy, though both types of energy may be produced simultane- 
ously and may be interdependent ; thus the growth of muscle is 



24 VETERINARY PATHOLOGY. 

dependent upon frequent and appropriate exercise (liberation of 
kinetic energy). 

Growth within the normal cell is dependent upon inherited 
tendencies and a sufficient supply of nutrition. Other functions, 
as motion, are apparently entirely governed by environmental 
stimuli plus the required nutrition. The growth of cells con- 
tinues until they, and the part they compose, become of such 
a size that the economic relation of surface and mass becomes 
disproportionate. The disproportionate relation of surface to 
mass is corrected by rapid cell division or cell dissociation. In 
either case the total cell surface is increased. According to 
Harris, ''Physiologic inertia" is of considerable importance in 
growth of cells. When a cell is stimulated to action, the action 
does not cease immediately when the stimulus is removed or 
suspended. Thus when a cell starts to grow, it tends to grow 
continually because of the ''physiologic inertia." Abnormal varia- 
tion in cell growth is characteristic of hypertrophy. 

Reproduction. — Cell reproduction is the process by which 
the number of cells is increased. The ultimate outcome of cell 
reproduction and cell growth, is to increase the mass or volume. 
Cell reproduction is not distinct and separable from cell growth, 
in fact growth always precedes division. Reproduction is one 
means of regulating the relation of surface to mass. Two types 
of normal cell reproduction have been described by cytologists. 
These methods are amitosis, (direct cell division), and mitosis, 
(indirect cell division.) 

1. DIRECT CELL DIVISION^ AMITOSIS, IS simple ccU divisiou in 
which the nucleus and cell body divide without any previous 
tiuclear changes. T^is type of cell reproduction or division is 
normal in some lower forms of life and possibly in some embry- 
onic tissues of higher animals. However, it is not very common 
in normal adult tissues of higher animals. The polynuclear 
leucocytes occasionally reproduce by amitosis ; endothelial cells 
are also thought to reproduce in the same way. It is possible 
that cells of any tissue may multiply by amitosis. Cells repro- 
duced by amitotic division are considered abnormal by most 
investigators. Direct cell division is especially evidenced in 
rapidly growing tumors, chronic inflammatory areas, leukemic 
tissue and many other pathologic conditions. The process is 
briefly as follows : There are one or more depressions in the 
nucleus which gradually extend until the nucleus is divided into 
two or more parts, (this is the origin of polynuclear cells ; possi- 
bly it may also account for the giant cells). After, the nucleus 



THE CELL. 



25 



has divided, each part migrates to a different part of the cell 
body and the cell body is so divided that one or more nuclei are 
found in each segment. Thus the process is completed. In 
some instances, one or even two centrosomes may be present. 




Fig. 2. — Amitosis, showing division of the nucleolus. 
/,. INDIRECT CELL DIVISION, MITOSIS, OR KARYOKINESIS, IS th^ 

usual mode of cell reproduction. The frequency and intricacy o\ 
this complicated process is indicative of the exactness of nature's 
methods. An equal division of the nucleus, or more specifically 




Fig. 3. — AmitoBiA. showing migration of the nucleoli to opoositft Dolea 

of the nucleus. 



of the nuclear chromatin, is apparently the object of this type 
of reproduction. It is more delicate and exact than direct cell 
division. The following four stages are recognized in indirect 
cell division, but they are not separate and distinct. 



26 



VETERINARY PATHOLOGY. 



A. Prophase. This is the preparatory stage. The nuclear 
chromatin which, in the resting cell, is an irregularly arranged 
net-work, becomes a continuous single thread, forming the so-' 




Fig. 4 — Division nf nnclpus 



called spirem or loose skein. The chromatin thread divides into 
a definite and even number of segments, (the number varying in 
different animals, but always constant in the same species) 
known as chromosomes. These chromosomes are equal in length 




fel 



Fig. 5.'— Division of cell. 



f 



and are usually bent like the letter ''u.'' The chromosomes are 
radially assembled around the central point in the nucleus, thus 
forming the monaster or single star. The nuclear membrane 
becomes less and less distinct as the spirem is forming and fin- 
ally disappears. As the nuclear changes are progressing, a 
centrosome becomes prominent either within the nucleus or in 
the cell body just outside the nuclear membrane. The centro- 



THE CELL. 



27 



some divides, the daughter centrosomes separate and wander to 
opposite sides of the nucleus. Radiating lines, known as mantle 
fibres, appear and extend from each centrosome to the chromo- 
somes. 




Fig. 6. Fig. 7. 

Fig-. 6. — Cell in resting stage. 

— Prophase showing division of centrosome. 



Fii 



B. Metaphase. During this stage the chromosomes are 
split or cleaved longtitudinally into daughter chromosomes 
apparently by the traction of the mantle fibres of the centro- 
somes. , 




Fig. 8. Fig. 9. 

Fi^. 8. — Prophase showing separation of centrosomes^ 
Fig. 9. — Metaphase. 



28 



VETERINARY PATHOLOGY. 



C. Anaphase, The daughter chromosomes are attracted 
along the mantle fibres until they reach the centrosomes around 
which they are ultimately assembled, forming an aster or 
star at either pole. This particular portion of the anaphase is 
designated the diaster or double star. There is also evidence 
of transverse indentation of the cell body near the median line. 




Fig. 10. 



Fig. 10. — Metaphase. 
Fig. 11. — Anaphase. 



Fig. 11. 



D. Telophase. The nuclear changes during this phase are 
practically the reverse of those occurring in the prophase, i. e., 
the chromosomes fuse forming a chromatin thread which later 
forms the chromatin network. The nuclear membrane appears 
and the centrosome loses its mantle fibres and may even entirely 
disappear. The cell body is completely divided by invagination 
from the margins, and then the daughter cells are completed and 
assume the appearance of their ancestors. 




Fig. 12. 



Fig 12. — Anaphase. 
Fif. 13. — Telophase. 



Fig. 13, 



THE CELL. 



29 



Morbid cell reproduction is especially evident in neoplasms 
and in hyperplastic formation. The type of reproduction in neo- 
plasms is variable, being normal or modified, direct or indirect. 
Indirect division is of most frequent occurrence in hyperplasia, 
the rapidity of multiplication being the only apparent difference 
from that occurring in normal reproduction. All variations of 
division occur in tumors. 

Motion. — Motility is that property of a cell which refers 
either to the intracellular movement of its parts, the position of 
the cell as a whole remaining fixed, or it signifies the inde- 
pendent movement of the cell. All movement is dependent 




Fig. 14. — Ciliated Epithelium, Trachea. 

Upon activity of the cell protoplasm. The cells of specialized 
tissues, except blood, are fixed i. e. not motile. 

Intracellular movement is due to the circulation or stream- 
ing of the protoplasm from one portion of the cell to another. 
This type of movement may become so extensive that the shape 
of the cell will be changed. It is common in the cells of lower 
forms of life as well as in some of the cells of higher animals. 
The specific cause of the intracellular protoplasmic circulation 
has never been positively determined but it is probably the result 
of a disturbed chemic equilibrium of the cell margins and their 



30 



VETERINARY PATHOLOGY. 



surroundings. Leucocytic amoeboid movement is due to intra- 
cellular protoplasmic circulation. Leucocytic immigration prob- 
ably is the result of chemic attraction, (positive chemotaxis), 
which stimulates the circulating protoplasm within the cell to 
constantly flow toward the point of greatest chemical affinity 
and finally the cell reaches that point. Leucocytic emigration 
is based upon the same principal except that the chemic in- 








1. rat. 



2. Horse. 

Fig. 15. — Spermatozoa. 



3. Man. 



THE CELL. 31 

fluence is negative, (negative chemotaxis), and the cell is forced 
away from the center of the disturbed chemic equilibrium. 

Ciliary movement is the wave like motion of small hair like 
protoplasmic projections of cells known as cilia. Ciliary motion 
occurring in migrating or wandering cells produces movement 
of the entire cell and in stationary cells, produces move- 
ment of fluids or semifluids that contact the cilia. In higher 
animals motion of entire cells as a result of ciliary movement 
is observed only in spermatozoa. The normal function of ciliary 
movement is to aid m propelling mucus in the respiratory tract, 
ova in the Fallopian tubes, spermatozoa in the vas deferens, etc. 
Ciliary movement is due to intracellular protoplasmic disturb- 
ances, at least it is the result of chemic influences. Over stimu- 
lation or disease may produce increased action and finally fatigue 
or paralysis of the cilia, or they may produce cessation of their 
action. The most extensive and important cell movement is 
noted in the highly specialized muscular cell. As the muscle 
cell maintains its relative position when contraction takes place, 
the movement is principally evident in the structures to which 
the muscle fibre is attached. The rate and extent of contraction 
vary in the different varieties of muscle. The spongioplasm is 
the active portion of the cell in contraction, the hyaloplasm being 
passive only in function. Nerve fibres terminate in end-organs, 
i. e., muscle plates, through which are transmitted impulses that 
produce muscular contraction. IMuscular movement is an in- 
dispensable function, as circulation and respiration are abso- 
lutely dependent upon it. Digestion and urination would also 
be suspended if muscular action were curtailed. Immobility may 
be the result of muscular fatigue or dissociation of motor nerves 
and muscle fibres, or be due to neuroses. jMuscular spasms 
are usuall}^ the result of violent stimulation of the motor nerves, 
although it may result from excessive stimulation of the muscle 
fibres themselves. 

Metabolism. — Metabolism is a term used to designate the 
processes included in nutrition or digestion, absorption, assimila- 
tion, katabolism, and excretion. These processes are the results 
of cell action. Metabolism includes two general processes, i. e., 
constructive metabolism or anabolism and destructive metabol- 
ism or katabolism. Active cells are constantly consuming foods 
and eliminating waste material. The quantity, quality and 
previous preparation of the nutritive substances required, varies 
according to the specialization and degree of action of cells. The 
leucocyte is relatively simple, i. e., it is a primitive type of cell. 
A leucocyte is not very selective in its food requirements. It 



32 VETERINARY PATHOLOGY. 

produces ferments that digest food substances, as well as necro- 
tic tissue as inflammatory exudate. The phagocytic action of 
leucocytes is largely dependent upon the fact that the substances 
phagocytized have been previously rendered inert. Connective 
tissue' cells are closely related to leucocytes in their power of 
producing digestive ferments. Endothelial cells produce fer- 
ments which aided by the leucocytic ferment, dissolve and devour 
thrombi and emboli. On the other hand nerve cells are quite 
selective in their food requirements and they have practically 
no power of producing digestive ferments. 

The foods required by cells are nitrogenous and non-nitro- 
genous. Nitrogenous nutrients are used in the construction and 
maintainance of the cell protoplasm. The non-nitrogenous foods 
are essential^ carbohydrates and fats which are consumed 
when energy, in the form of either heat or motion, is liberated. 
When non-nitrogenous foods are consumed in excess, some of 
them may be stored as glycogen in the liver, or as fat in the 
various parts of the body, thus producing glycogenic or fatty in- 
filtration. The consumption of nitrogenous food in excess may 
result in overwork of nitrogenous excretory organs as in induced 
albuminuria. Insufficient supply of carbonaceous food produces 
disturbed metabolism, because of the necessary conversion of 
nitrogenous food or nitrogenous cell constituents into carbon- 
aceous substances, in order that the body energy may be main- 
tained. Diminished supply of nitrogenous foods is temporarily 
compensated for by consumption of the protoplasm of the body 
cells. If the nitrogenous food supply is materially diminished 
for a long time or entirely withheld, the body cells atrophy, 
degenerate, and ultimately die. 

The waste products are also divisible into two classes, nitro- 
genous and non-nitrogenous. The nitrogenous waste substances 
are urea, or some allied product. They represent katabolic pro- 
ducts, i. e., the results of destructive changes in the cell proto- 
plasm. The carbohydrates and fats are almost entirely converted 
into energy ; carbon dioxide and water being the chief katabolic 
products. 

Irritability. — Irritability is the property of certain cells which 
enables them to respond to stimuli. Stimuli may be chemic, 
thermic, electric or mechanic. The property of irritability is 
vested especially in nerve cells, although other cells are slightly 
irritable, e. g., muscle cells. The degree of sensitiveness varies 
greatly in different species of animals and to a less extent in dif- 
ferent individuals of the same species. Thus the thoroughbred 
horse has a more sensitive skin than the draft horse. Irritability 



THE CELL. 33 

is a very important property because it is the means through 
which the nature of environments is recognized. Many of the ac- 
tivities of the body are responses to impulses resulting from stim- 
ulation of irritable cells. Irritability is the property of cells which 
enables an animal to communicate with its environments as, 
sight hearing, smell, etc. Irritability may be intensified or 
diminished by pathological processes. Thus chemic variations, 
resulting from katabolism in tissues affected with inflammatioUj 
produce increased irritability or intensify stimulation of nerves, 
and is manifested by hyperasthesia or by pain. Anemic and 
venous hyperemic tissues are usually less sensitive than normal 
tissues because of the accumulation of waste product that tend 
to inhibit impulses or diminish irritability. Correlation of the 
cell to the entire organ is of considerable moment, and is de- 
pendent upon irritability and response to stimuli. 



CHAPTER II. 
GENERAL CONSIDERATION OF DISEASE. 

DEFINITION. 
CLASSIFICATION as to. 
Time affected. 
Inherited. 

Definition. 
Predisposition. 
Tumors. 
Neuroses. 

Malformations — not rare.. 
Infections — rarely if ever. 
Acquired. 

Definition. 

Antenatal — (congenital) — Exanthema. 
Postnal — Spavin. 
Extent ill affected animals. 
Local — inflammation. 
General — anthrax. 
ETIOLOGY. 

Predisposing. 

Heredity — Epiplepsy. 
Inbreeding — General debility. 
Age — Canine and colt distemper, blackleg. 
Sex — Males urethral calculi; females, peritonitis. 
Genus — Hogs, cholera; cattle, blackleg. 
Breed — Clydesdale, laminitis; jersey tuberculosis. 
Color — White animals, sunburn. 
Location — Pica. 
Climate — Contracted hoofs. 
Season — Pneumonia, insolation. 
Food and Watef — Indigestion. 

Occupation — City horses, foot disease; dairy cow, udder disease. \ 
Effects of previous disease — Purpura hemorrhagica. ] 

Exciting. i 

Mechanic — Fractures, dislocations, sprained tendons. 
Physic. 

Electric — Lightning stroke, electric wires. 
Thermic ; Burns, overheat, freezing. 
Chenv^e.. 

Inorganic — Saturnism. 
Organic — Sorghum poisoning. 
Poisonous plants — Loco, hemlock, larkspur. 
Poisons secreted by snakes, bees, etc. 
Parasitic. 

Bacteria — Glanders, tuberculosis. 
Yeast — Epizootic lymphangitis. 
Moulds — Pulmonary mycosis. 
Protozoa — Tick fever. 
Vermes — Trichinosis. 
EXTENSION. 

Natural channels — Digestice, urinary^ etc. 
Continuity — Along a muscle, etc. 

Contiguity — From muscular to connective tissues, etc. 
Blood — In plasma, leucocytes or red cells. 
Lymph — In plasma or leucocytes. 
Nerve -fibres — Aloncjspaxone. 
TERMINATION. 

34 



GENERAL CONSIDERATION OF DISEASE. 35 

Health has been defined as that condition in which the normal 
structure and functions of all the component parts of an or- 
ganized being are maintained. 

Disease is a functional or structural deviation from the normal. 
It is that condition in which an organism cannot accustom itself to 
its environments, Heahh and disease are, however, only relative 
terms, because of the difficulty of determining a normal standard. 
The two conditions necessarily overlap. 

Diseases may be class?iied in many ways, as local and general, 
infectious and non-infectious, inherited and acquired, etc. 

Inherited diseases are those transmitted from the parent in 
spermatozoa or ova and are present at the time of fertilization. Cer- 
tain characteristics are transmitted from parent to offspring such as 
genus, breed and individual peculiarities. Thus horses have peculi- 
arities so fixed and constant that they are transmitted to their off- 
spring and differentiate them from other species of the genus Equus. 
Breeds are dift'erentiated by certain peculiarities ; thus Jersey cattle 
are brown to light fawn in color with a brown muzzle, horns turned 
in and up, they are small, lean, dish faced, etc., all of which are 
peculiarities that distinguish them from other breeds of cattle. 
There are individual peculiarities, some of which are the result 
of the fusion of parental characteristics ; thus the offspring may 
be of solid color, the result of the fusion of different parental 
colors, (color blending), or they may be piebald, indicating fail- 
ure of color blending (mosaic coloring). The extent of intensi- 
fication of inherited generic, breed or individual peculiarities de- 
pends upon the prepotency of the parental stock. This pre- 
potency depends upon the length of time that the type has 
existed under similar circumstances. The foregoing illustrates 
what is meant by the term "heredity", and demonstrates that 
the breeding of stock is a science. 

Diseases are rarely inherited, first, because diseased spermato- 
zoa and ova are probably incapable of fertilization, and second, 
there is always a tendency to abort when the embryo or foetus 
is diseased. A predisposition may be inherited, i. e., the progeny 
of diseased parents may be more susceptible to disease than the 
progeny of a healthy parentage. Infectious diseases are very 
rarely inherited. It has been demonstrated that spermatozoa 
are not phagocytic in action and probably ova have no phago- 
cytic tendencies ; the latter, however, has not been proven. The 
quantity of semen and the number of spermatozoa per given 
volume varies in different animals and in the same animal under 



36 VETERINARY PATHOLOGY. . 

different conditions. Loeb estimated that the average human 
seminal ejaculation contained about 226,000,000 spermatozoa. 
The average seminal ejaculation of a dog probably contains 
about the same number of spermatozoa as that of the human. 
Lewis found that one stallion ejaculated 65 cc. of semen during 
one service, each cmm. of which contained approximately 131,- 
750 spermatozoa; another stallion ejaculated 90 cc. of semen dur- 
ing one service, each cmm. of which contained approximately 
225,000 spermatozoa. The quantity and the number of sperma- 
tozoa per given volume of semen ejaculated during one service 
of the bull has not been determined, at least the information has 
not been found in the available literature. However, it is reason- 
able to suspect that the number of spermatozoa ejaculated dur- 
mg a single service by the bull is equal to the number ejaculated 
by a stallion during a single service. It is difficult to collect 
the entire discharge of semen of a boar, but Lewis obtained 100 
cc. from a single service of a boar and by repeated examinations 
he has determined that the semen from boars contains more 
spermatozoa per given volume than that from stallions. There 
would, therefore, be less chance for fertilization with an infected 
spermatozoon in the horse, ox and hog than in man. Suppose 
there were 1,000 tubercle bacilli infecting 1,000 spermatozoa that 
were ejaculated by a bull in one service, then there would b€ 
one chance in about 12,000,000 of an infected spermatozoon 
fertilizing an ovum, assuming that one seminal ejaculation of 
the bull contains approximately the same number of spermatozoa 
as one seminal ejaculation of a stallion. The chance is so slight 
that it need not be considered. The offspring of animals affected 
with some infectious diseases are more susceptible to those dis- 
eases. For example, calves of tuberculous parentage are more 
susceptible to tuberculosis than calves of non-tuberculosis 
animals. 

Neoplasms or tumors are occasionally inherited or at least 
there is an inherited predisposition to them. Dr. A. F. Meredith 
of Lincoln, Kansas, submitted a tumorous growth for examina- 
tion that was obtained from the left eye of a mule. The dam 
of the mule, as well as four of her brothers and sisters had a 
similar defect of the same eye. Cadiot refers to a family of dogs 
in which there wiere carcinomata of the mammae for two successive 
generations. 

Malformations, though usually of congenital origin, are 
probably more frequently inherited than is any other type of 
disease. Thus a cryptorchid stallion was used for breeding 
purposes in a certain locality in Illinois and about 20% 



GENERAL CONSIDERATION OF DISEASE. 37j 

of his male colts were cryptorchids. About 5% of tHe male 
progeny of one of Missouri's most famous boars, Chief Tecum- 
seh II, were cryptorchids. Libert}- Chief and Chief I Know, 
two boars sired by Chief Tecumseh II, were noted boars and 
from 3 to 5% of their male get were cryptorchids. Chief Per- 
fection II, also sired by Chief Tecumseh II, was the sire of Che- 
rokee Perfection which in turn sired about 3% of cryptorchids. 
Thus this structural defect appeared in at least three genera- 
tions. A female Belgian hare having one ear, produced a large 
number of young of which more than 50% had only one ear. 

Epileptic domestic animals and those affected with other 
nervous disorders are usually destroyed or at least are not bred, 
hence the statistics of inherited nervous diseases in domestic 
animals are very meagre, but there is little doubt that such 
diseases, or at least a predisposition to them, is inherited. La 
Notte recorded hereditarv epilepsy in the progenv of two epi- 
leptic bulls, the disease becoming evident in the females after 
they had given birth to their first calves, and in bulls soon after 
they were put into service. 

Some other diseases are inherited, thus ; periodic ophthalmia 
has, in many instances, occurred in, and affected practically an 
entire familv of horses. There is a predisposition to spavins, 
splints and ringbones in certain strains of horses. This is due 
to inheritance of ^structural or conformation defects. 

ACQUIRED DISEASES. 
The life of mammals is conventionally divided into two 
periods, the ante-natal or intrauterine, and the post-natal or 
extrauterine. Acquired diseases are those contracted after 
fertilization and hence may be ante-natal, (congenital) or post- 
natal. 

Ante-natal or Congenital diseases are those contracted be- 
tween the time of fertilization and birth. Some infectious diseases 
are congenital, for instance, marked lesions of tuberculosis were 
found by the writer in 1900 in a three day old calf, and two 
authentic reports of similar cases have been received since that 
date. (These cases were not considered as inherited for the 
reason heretofore given, and in all three cases lesions of tubercu- 
losis were found in the uterus and adjacent tissues of the cows.) 
Infectious disease^ are seldom transmitted from the mother to 
the foetus because of the relation and anatomical structure of the 
placental membranes. The female is usually either sterile or 
aborts if the uterus or the accessory parts are diseased, while 
the male is not likely to be productive if the genital organs are 
diseased. Exanthematous diseases are frequently con-genital. 



38 VETERINARY PATHOLOGY. 

Teratomata and other malformations are diseased conditions and 
are usually of congenital origin. 

Post-natal diseases are those contracted at any time during 
the life of the animal after birth, as laminitis, actinomycosis, and 
spavin. 

In classifying diseases according to extent, two groups are 
usually described, viz : — , local and general. 

1. A LOCAL disease is one that af¥ects a part or organ ; as urethral 
calculi, pulmonary anthracosis, etc. Local diseases proper remain 
localized although the term is used in a broader sense to desig- 
nate a circumscribed, local, morbid process that may later be- 
come generalized. Thus ; tubercular infection of a group of 
lymphatic glands is frequently spoken of as localized tubercu- 
losis. 

2. A GENERAL discasc, strictly speaking, is one invoking the en- 
tire animal body, as anemia, but in a more restricted sense it is 
used to designate the involvement of several parts or organs. 

Etiology. — Disease has been defined as an inharmonious 
relation between an individual and its environments. This 
definition is indicative of the various factors concerned in the 
production of mor^bid processes. The causes of disease may be 
conveniently subdivided into two groups, viz. ; predisposing causes 
and exciting causes. 

PREDISPOSING CAUSES. — Predisposing causes are those condi- 
tions or environments whch render animals more suscept- 
ible to disease. 

It has long been recognized that many diseases of domestic 
animals are due to induced variations of species that result from 
selection by breeders. New breeds of the various animals are 
produced so rapidly, that the individuals of the new breeds are 
more susceptible to disease. 

Retrogressive changes in anatomical structures predispose to 
disease. The tarsal joint of the horse is gradually changing 
from an active to a passive structure ; this change results in a 
tendency to ossification and ankylosis or spavin formation. Pro- 
gressive changes in various structures are responsible for some 
diseased conditions, viz., navicular disease in the horse, or dairy 
breeds having large udders, are more susceptible to mammary 
diseases. Several breeds of horses are characterized by small 
heads and especially diminished facial bones, a conformation 
that predisposes to dental diseases. 

Inbreeding has been a cause of decreasing the resistance of 
animals to disease. 

Age. The age of animals is an important predisposing factor 



GENERAL CONSIDERATION OF DISEASE. 39 

in the causation of disease. The very young animal is struc- 
turally more delicate than the matured animal. Tissues are more 
or less permeable to the various bacteria, and until the young 
acquire an immunity, i. e., establish a resistance, they are more 
or less influenced by bacterial activity in their tissues. There 
are some diseases, however, that affect only young animals, as, 
canine and colt distemper, while other diseases occur primarily 
or only in adults as carcinomata land bursattae. 

Sex is of consequence in the occurrence of disease. Parturi- 
tion predisposes females to disease. Males are especially suscept- 
ible to urethral calculi. 

Genus may be a characteristic factor in the predisposition to 
disease. Glanders is a disease of the genus equus, caseous-lymph- 
adenitis of the genus ovis, canine distemper of the genus canis, 
rinderpest of the genus bovis. 

Breed. — ^There are certain peculiarities of different breeds of 
animals that are inducive to disease, thus the original Clydesdale 
horse is not resistant to laminitis ; the thoroughbred having a 
nervous temperament is more susceptible to heart disturbances ; 
the jersey cow with a diminished breathing capacity is more 
liable to pulmonary tuberculosis. 

White or light colored animals are more susceptible to der- 
matitis and are more affected by flies than those of darker color. 
In certain locations there are no white hogs because the hogs 
in those locations feed upon the roots of Lacuanthis tinctoria, 
which causes a pink discoloration, (hyperemia), of their bones 
and causes sloughing of the feet in all except black hogs. 

Individuals of a resistant strain are sometimes especially sus- 
ceptible to certain diseases. 

Location. — The soil of a locality may be deficient in some 
necessary ingredient or contain some noxious constituent. Some 
localities may be continually damp and muddy, others dry and 
dusty, and still others abound in objectionable gases and odors. 
Any of the above conditions naturally diminish the resistance of 
animals ; thus pica exists in localities in which the soil is prob- 
ably deficient in some ingredient, scratches and thrush are com- 
mon where mud abounds ; broken and cracked feet in dry dusty 
regions, and nasal catarrh where irritating odors are common. 

Climate definitely influences the hairy covering of animals. 
In Angora, not only goats but also collie dogs and cats have 
fine fleecy hair. Mules kept in mines constantly for a long time 
become covered with velvety hair like that of a mole. 

Season. — Some diseases are more common In certain seasons. 



40 VETERINARY PATHOLOGY. 

Thus pneumonia is more prevalent during the seasons of sudden 
change as early spring and late fall. 

Occupation.— The city express horse is particularly liable to 
diseases of the feet, the thoroughbred to rupture of the heart 
or blood-vessels, the dairy cow to udder diseases, the house 
dog to indigestion, etc. 

Food and Water. — Excessive, insufficient or unwholesome food 
and water, also irregularity of feeding or watering are fre- 
quent causes of depressed condition of animals. In Holstein 
an enzootic anemia destroys hundreds of suckling pigs annually. 
The pigs are apparently normal until about two weeks of age. 
The cause is probably improper food and a predisposition result- 
ing from excessive stimulation of the reproductive function of 
the sow. Variegated color of parrots is produced by feeding 
green parrots fat from siluroid fishes. Colic is essentially a 
dietary disease. 

The effects of previous disease frequently leaves an animal 
in a depleted condition, thus petechial fever is frequently a 
sequel of pneumonia or "stable fever" (catarrhal fever). 

Overzi'ork, lack of exercise, variable temperatures, and other 
minor causes all have their influence in depressing the animal 
body. 

Imitation. — Some animals, colts especially, have 0. tendency 
to imitate what other horses do, thus colts allowed to run with 
cribbing horses occasionally become cribbers. 

EXCITING CAUSES of disease are those acts or agencies which 
directly and specifically produce disease as falling, sunlight, 
chemic substances and infection. 

Mechanic, physic, chemic and parasitic agencies are the principal 
exciting causes of disease. 

Mechanic. — Diseases are produced mechanically by break- 
ing the continuity of involved tissues, by com^pression, or by 
changing the relations of anatomical elements. The condition 
resulting from a break in the continuity of a surface soft tissue 
is termed a wound, of sub-surface soft tissue, a rupture and of 
osseous tissue, a fracture. Compression may cause bruising or 
crushing depending upon the mechanical object inducing the in- 
jury, and the amount of pressure exerted. Luxations or dis- 
locations are the result of changed relations of bones^ tendons 
and ligaments. Volvuli and intussusceptions are the result of 
changed relations of the intestine. Hernia is a condition in 
which there is a changed relation, caused by a break in the 
continuity of one tissue which permits an adjacent tissue or 
structure to protrude or sacculate through it. 



GENERAL CONSIDERATION OF DISEASE. 41 

Dogs are more frequently injured by biting than other ani- 
mals although they may inflict lacerated wounds in other ani- 
mals especially hogs. Horses more frequently than other ani- 
mals become injured by pawing, rearing, kicking, falling and 
colliding with foreign objects. The majority of barbwire 
wounds are the result of pawing over or through a wire fence. 
Rearing frequently results in straining the calcaneo-cuboid liga- 
ment thus producing a curb. Slipping may cause the straining 
of tendons, thus producing curbs and spavins as well as ten- 
donitis. Falling may produce strained tendons and is the usual 
cause of dislocations, rupture, hernia, volvulus and fractures. 
Runaway horses and mules frequently collide with fences, trees, 
buildings, and various vehicles, as buggies, wagons, street cars, 
etc., and thus produce a variety of injuries. 

Ill-fitting shoes are responsible for contracted feet, strained 
tendons and ligaments, speedy cuts and bruises by interfering. 
Illfitting collars produce galled shoulders, sore neck, cerebral 
venous congestion and sweeney. Illfitting harness produces 
Sweeney, sore neck, sore back, galled sides, rump and tail, an 
illfitting bridle causes irritation of the mouth, injuries to the 
eyes, the ears and the throat-latch region, and poll evil. Except- 
ing the sore mouth, illfitting halters produce the same results as 
illfitting bridles.- Illfitting saddles produce sore backs, sitfasts, 
injurv in the region of girth and bruises resulting in fistulous 
withers. 

Attendants may inflict injuries of various types. Several 
cows in a dairy recently observed, were all lame in the right 
hind leg. Upon closer inspection the right tarsal joint was 
found enlarged and sensitive. One man had been milking all 
the affected cows and finally admitted that he had either kicked 
or struck each lame cow upon the tarsal joint. 

Bandages are frequently so tightly wound upon a part that 
they obstruct circulation thus producing venous congestion, 
which predisposes to infection. Some cases have been observed 
in which splints improperly applied to support a part have 
resulted in venous congestion, oedema and necrosis. Careless 
individuals will place rubber bands upon dogs' tails, ears, and 
feet to see the animals remove them. The dog will sometimes 
fail to remove the rubber band, which, by pressure, may divide 
the skin and soft tissues, and finally cause the portion distal 
to the band to become necrotic and slough. 

Shooting occasionally causes mechanical injury to animals 
In pastures, especially during the hunting season. This is more 
frequently the source of injury during a war, and a knowledge 



42 VETERINARY PATHOLOGY. 

of the various types of bullets and wounds inflicted by same 
is of considerable importance to army veterinarians. 

Powdered glass, which is sometimes maliciously incorporated 
in food for the purpose of destruction of life, may excite gastric 
and intestinal inflammation. Sand is sometimes consumed in suf- 
ficient quantities, by animals, grazing upon sandy soil, to mechan- 
ically interfere with digestive functions, and mechanically injure 
the gastric and intestinal membrane. Nails, wire, staples, etc., 
are frequently ingested with food by animals, especially cattle, 
which objects may abraid and cause injury by producing abra- 
sions of the mucous membrane or even by puncturing the wall 
of the digestive tract, thus establishing such inflammatory dis- 
turbances as peritonitis, pleurisy, pericarditis, etc. 

Various mechanical contrivances such as operating tables, 
throwing harness and hobbles, used in subduing fractious ani- 
mals or confining animals for operative procedure may produce 
injury. 

1. Physic. — Temperature variations, not only predispose to 
disease, but may also become an exciting cause. Excessively high 
temperature is likely to produce overheat, (insolation, heat 
prostration). Overheat or heat prostration is frequently ob- 
served in fat hogs having little or no shelter in the summer 
time, or in hogs being hauled in wagons or cars, or being driven 
in herds to market. It is also frequently observed in horses 
worked on pa^vements in cities during the summer months. 

Local application of excessive heat produces burns. The 
lesions produced in local burns, vary according to the degree 
of temperature, the length of time applied and the tissue resis- 
tance. Three grades of lesions, of local burns, determined by 
the degree of temperature, may be described. First, short expos- 
ure to a temperature of from 50° to 60° C. produces an hyper- 
emia or a burn of the first degree ; second, exposure to a tem- 
perature of 60° to 80° C. for a short time produces inflammid- 
tic">n, characterized bv a serous exudate that accumulates in the 
malpighian layers of the epidermis forming vesicles or blisters; 
third, an exposure to a temperature above 80° C. for a fbrief 
period, produces necrosis, the dead tissue becoming dry and 
hard. Burns involving one-fourth to one-third of the cutaneous 
surface frequentl)^ terminate fatally as a result of excessive heat, 
hemolysis of the red corpuscles, increased heat dissipation and 
other disturbed cutaneous functions. 

Excessively low temperature may diminish the bodv tem- 
perature, of warm blooded animals, to the extent that the func- 
tioning is modified or inhibited sufficiently to result in death. 



GENERAL CONSIDERATION OF DISEASE. 43 

Animals are naturally protected from the effects of low tem- 
peratures, in dry weather, by their coat of hair, fur, wool or 
ieathers. When their protective coat becomes wet it no longer 
prevents heat dissipation consequently animals having no shel- 
ter, as ranch horses, cattle, and sheep, frequently die in great 
numbers during the earl}^ cold spring rains. 

The local lesions caused by low temperature are practically 
the same as those resulting from exposure to high temperature. 
Thus exposure to a mild, low temperature produces hyper- 
emia ; exposure to freezing temperature produces inflammation 
accompanied by a serous exudation but the exudate rarely 
accummulates and forms a vesicle as in burning. Exposure to 
extreme low temperature produces necrosis, the frozen tissue 
becoming dry and hard. 

Animals are most frequently exposed to temperatures suffi- 
ciently high to produce insolation in the daytime, in the tropi- 
cal or temperate zones, although overheat is sometimes observed 
during the night. Exposure to temperatures that produce local 
burning usually occurs in conflagrations of buildings. Scores 
of animals die, in the spring, on ranges or large pastures, in the 
temperate zone, as a result of dim.inished body temperature in- 
duced by exposure to cold rains. These animals are usually 
depleted because- of insufficient or non-nutritious food. Their 
coat of hair or wool becomes saturated with water and thus the 
body temperature regulation is disturbed. Lesions produced by 
low temperatures are evident only in regions and seasons, where 
there is a low atmospheric temperature. Local freezing usually 
occurs in extremities as the ears, tail and feet. 

2. Photic. — Exposure to sunlight frequently produces derma- 
titis, especially in those animals having a thin, light colored skin. 
White hogs are quite seriously affected by sunburning, in some 
localities. This peculiarity prohibits the raising of white hogs, 
in certain districts in Africa and Central America. R. Paine, F. 
R. C. V. S., of the Department of Agriculture of Cape Colony, 
in the Journal of Comparative Pathology and Therapeutics, 
Part 1, Vol. XXI, reported some cases of dermatitis in cattle, 
that were undoubtedly the result of exposure to sunlight. D. M. 
Campbell observed about 40 Duroc Jersey pigs affected with derma-, 
titis induced by sunlight. 

Direct or reflected sunlight is also injurious to the eyes of 
domestic animals. The injurious effects are noticed more especi- 
ally in animals driven upon macadam thoroughfares or over 
light colored soil. Electric and gas lights have also been 
found to be injurious to the eyes of various animals especially 



44 VETERINARY PATHOLOGY. 

when the lights are allowed to shine directly into their eyes. 
Epilepsy has been produced in horses by sudden exposure to 
intense light. 

The immediate cause of the effects of exposure to sunlight 
upon the skin is not known but is thought to be the result of 
the action of the actinic or chemic rays. The effects of expos- 
ure to light upon the eyes is excessive stimulation which pro- 
duces exhaustion thus predisposing to, if not directly exciting 
disease. 

3. Electric. — Animals are susceptible to the action of elec- 
tricity. Horses are especially susceptible to its influences, a 
direct current of 500 volts, 100 amperes, is sufficient to kill a 
horse, and an alternating current of 160 volts is destructive to 
medium sized dogs. 

Contact with electricity may be the result of lightning, and 
charged electric wires, or rails. Horses and cattle frequently are 
struck by lightning while in pastures, and animals used in cities 
are occasionally accidentally brought in contact with electric 
currents. Depending upon the amount of electrical current, the 
results may be a slight singeing of hair, burning, or laceration 
of tissues in general. Carcasses of animals destroyed by electri- 
cal currents have also been observed in which no lesions could 
be found. On examination of carcasses of animals dead of 
lightning stroke, there is usually more or less singeing of the 
hair, hyperemia and hemorrhages along the course of the cur- 
rent. 

Chemic. — Chemic substances capable of producing disease are 
very common and may have their origin from the mineral, veg- 
etable or animal kingdom, and are inorganic or organic. It is 
probable that practically all chemic substances may, under cer- 
tain conditions, be injurious to the tissues of the various animals. 
Some chemicals are always injurious, others may become in- 
jurious by chemic change induced by the tissue juices. Those 
chemicals capable of producing deleterious effects in the animal 
tissues are poisons. (Poisons are substances which when taken 
internally or applied externally alter health or destroy life w^ith- 
out acting mechanically or reproducing themselves.) 

According to their modes of action, poisons have been classi- 
fied as follows: 1. Corrosive poisons, (caustics and irritants.) 

The action of fhis group varies from the production of a 
simple hyperemia to necrosis. The most common agents are 
mercury, arsenic, sodium and potassium hydroxide and the min- 
eral acids. 

2. Parenchymatous poisons. This .2"roujD oroduc/^^; tissue 



Common Name. 

Ergot 

Stink Horn 
Bunch Flower 
White Hellebore 
Calif. Hellebore 

Pokeroot 
Corn cockle 

Monkshood 
Wild Monkshood 
Wild Monkshood 
Larkspur (dwarf) 
Larkspur (purple) 
Larkspur (Wyoming) 
Larkspur (tall) 
Mayapple 

Wild blackberry 

Wooly loco 

Stemless loco 

Rattlebox 

Wild or blue pea 
Wild or blue pea 
Alsike clover 
Red Buckeye 
Horse chestnut 
Ohio Buckeye 
Calif. Buckeye 
Water Hemlock 

Oregon Water 

Hemlock 
Poison Hemlock 
Broad leafed laurel 
Narrow leafed 

laurel 
Great laurel 
Black ni.(.'Utshade 

Spreading night- 
shade 
Horse Nettle 

Jimson weed 

Tobacco 

Potato 

Cocklebur 

Cocklebur 
Sneezeweed 

Death Canas 
Sorghum 

Kaffir corn 
Castor bean 



ORDER OR 
FA3irLY 

Hypocracaea 
Phallaceae 
^?eia.Iithacae 
Malanthacea 
Malanthacea 

Phytolaccaceae 
Caryophyllacea 

Ranunculaceae 
Ranunculaceae 
Ranunculaceae 
Ranunculaceae 
Ranunculaceae 
Ranunculaceae 
Ranunculaceae 
Berberidaceae 

Prunaceae 

Leguminosae 

Leguminosae 

Leguminosae 

Leguminosae 

Leguminosae 

Leguminosae 

Aesculaceae 

Aesculaceae 

Aesculaceae 

Aesculaceae 

Umbilliferae 

Umbilliferae 

Umbilliferae 

Ericaceae 

Ericaceae 

Ericaceo.o 
Solanaceae 

Solanaceae 

Solanaceae 

Solanaceae 

Solanaceae 

Solanaceae 

Compositae 

Compositae 
Compositae 

Melanthaceae 
Gramineae 

Gramineae 
Euphorbiaceae 



BOTAIVICAL, NAME. 



GENUS 

Claviceps 

Uathrus 

Chrosperma 

Vevatrum 

Vevatrum 

Phytolacca 
Agrostemma 

Aconitum 

Aconitum 

Aconitum 

Delphinum 

Delphinum 

Delphinum 

Delphinum 

Podophyllum 

Prunus 



SPECIE 

purpura 

columnatus 

muscaetoxicum 

vlvide 

californlcum 

americana 
githago 

napellus 

3olumbianum 

uncinatum 

tricorne 

menziesil 

geyeri 

glaucum 

peltatum 

serotina 



Astragalus mollisimus 

Aragallas (Oxytropis) lamberti 



Crotalaric 

Lupinus 
Lupinus 

Aesculus 
Aesculus 
Aesculus 
Aesculus 
Cicuta 

Cicuta 

Conium 
Kalmia 
Kalmia 

Rhododendron 
Solanum 

Solan um 

Solanum 

Datura 

Nicotiana 

Solanum. 

Xanthium 

Xanthium 
Helenium 

Zygadenus 
Andropogon 

(Hack) 
Andropogon 
Ricinus 



sagittalis 

leucophyllus. 
argentus 

pavia 

hippocastanum 

glabra 

California 

maculata 

vagans 

maculata 

latifolia 

angustofolla 

maximum 
nigrum 

nl.grum 

trifiorum 

carolinense 

stramonium 

tobacum 

tuberosum 

canadense 
glabratum 

venenosus 
Sorghum 

Sorghum 
communis 



INSERT I. 



PART OF 

PLAJfT 
POISOXOUS 

entire 

entire 

bulbs 

leaves 

leaves and seed 

root 

entire seeds 

especially 
roots and leaves 
roots and leaves 
roots and leaves 
seeds and leaves 
seeds and leaves 
seeds and leaves 
seeds and leaves 
leaves 

leaves 

leaves and stem 

leaves and stem 

leaves and seeds 

pods and seeds 
pods and seeds 

leaves and fruit 
leaves and fruit 
leaves and fruit 
leaves and fruit 
roots 

roots 

roots 
. leaves 
' leaves 

leaves 

leaves, roots and 

fruit 
leaves and fruit 

leaves and fruit 

leaves and fruit 

leaves and fruit 

tuber 

cotyledons 

seed 

entire plant 

bulbs and leaves 
leaves 

leaves 
seed 



POISONOUS 
PRIIVCIPLE 

Ergotine 



Veratrine 

Veratrine 

Phytolaccine 



Aconitine 
Aconitine 
Aconitine 



Podophyllin 

(Berberine) 
Hydrocyanic acid 

Barium Chloride 

Barium Chloride 

Unnamed alkaloid 

Lupinin 
Lupinin 

Aesculin 
Aesculin 
Aesculin 
Aesculin 
Conine 

Conine 

Conine 

Andromedotoxin 

Andromedotoxin 

Andromedotoxin 
Atropine 

Atropine 

Atropine 

Atropine 

Nicotine 

Solanin 



Hydrocyanic acid 

Hydrocyanic acid 
Ricin 



ANIIVIAtS 
AFFECTED 

all 

Hogs especially 

cattle especially 

all 

all chiclsens 

(seed) 
sheep 
all chickens 

especially 
all 
all 
all 

cattle and sheep 
cattle and sheep 
cattle and sheep 
cattle and sheep 
cattle 

cattje 

Cattle, Horses 

and sheep 
Cattle 

Cattle and Horses 

sheep 

sheep 

horses 

all 

all 

all 

all 

all sheep and 

cattle 
all sheep and 

cattle 
all 

cattle and sheep 
cattle and sheep 

cattle and sheep 
all 

all 

all 

all 

all 

horses and 

sheep 
pigs, cattle 
and sheep 
pigs 
horses, cattle and 

sheep 
sheep and cattle 
cattle 

cattle 
all 



LOCATION OB DISTRIBUTION 

Universal 
Southern States 
Eastern U. S. 

Eastern and Northern U. S. 
California 

Eastern 2/3 of U. S. 
Eastern 2/3 of U. S. 

Universal garden plant 
N. "W. America. 

North Central U. S., Ga., Pa- 
Ohio, Ind., Pa., Ky., N. C, Ga., Ark. 
N. W. U. S. and S. W. Can. 
"Wyoming and N. Colo. 
N. W. U. S. 
Que., Fla., Tex. 

Middle Atlantic States, Dak., Kans., 

Tex. 
Plains U. S.. Mex. and Can. 

Plains U. S. Mex. and Can. 

N. Car., Fla., S. Dak., Ark., Mex. 
Western IJ. S. especially Mo. river 

valley. 
Uplands and foothills. 
Central U. S. uplands and foothills. 
Central U. S. uplands and foothills. 
Gulf and middle states, Va. to Fla. 

N. Eng., N. T., N. J. 
Ohio, Pa., Ala., Mich., Okla., Neb. 
California. 
Eastern and Gulf States, N. Mex. 

N. W. U. S. 

N. E. U. S. and California. 

Allegheny district, Fla., La. 

N. E. U. S. Ga., Mich., Hud. Bay, 

New Found. 
Allegheny Mts., Nova Scotia, Ont. 
Universal 

Ont. N. W. Ter., Kans., Ariz. 

Central U. S. also Eastern U. S. 

Universal 

Universal 

Universal 

Universal 



Georgia, N. Eng., 
Universal 

Western U. S. 
Plains especially. 

Plains especially. 
Universal 



Fla., Neb., Mex. 



GENERAL CONSIDEIL^TION OF DISEASE. 45 

degeneration, especially parenchymatous and fatty degenera- 
tions. The most common parenchymatous poisons are the tox- 
ins, endo-toxins, ptomains, leucomains, phosphorous and silver. 
3. Hemic poisons. These act principally upon the red blood 
corpuscles and may inhibit combination of hemoglobin and 
oxygen, and cause disintegration of the cells and even produce 
thrombosis. The principal agents that combine with hemo- 
globin and thereby produce disintegration of the red cells, are 
carbon monoxide, sulphuretted hydrogen, hydrocyanic acid, the 
chlorates, and mercury. 

4. Xerve and Cardiac Poisons. These may produce paraly- 
sis by over-stimulation of nerve centers, or they may produce 
variation in the rate and force of the heart beat. Narcotics, 
such as atropine and solanin are types of neurotoxic poisons. 
Potassium salts depress the rate and increase the force of the 
heart action. 

A poisonous drug may act in a variety of ways depending 
upon the form of the drug, size of dose and method of adminis- 
tration. 

The following are the more common inorganic poisons : — 
arsenic, mercury, sodium, potassium, lead, copper, chlorine, and 
and the various oxides, salts, acids and bases formed from 
them. 

Many organic compounds are responsible for poisoning in 
animals as phenol, iodoform, picric acid, hydrocyanic acid. In 
fact most of the medicinal organic compounds are poisonous in 
large doses. 

There are many plants that are responsible for extensive 
losses of live stock in all parts of the United States, Canada and 
Mexico, and are most extensive in range districts. Colorado 
and jMontana have had losses aggregating $200,000.00 annually. 
in live stock, from plant poisoning. The following table gives 
the common and botanical names of plants that most frequently 
produce poisoning in animals. (See insert No. 1.) 

These plants are not all poisonous during their entire 
development. The cocklebur is most poisonous in the earlier 
stage of development, that is, at the time the cotyledons come 
through the soil and for two or three days after the plant is up. 
Lupines are harmful principallv while the seeds are maturing. 
Larkspurs are harmful only until the flowers appear. Dry sea- 
sons are usually most favorable to the formation of poison- 
ous principles in plants. Ergot develops most extensively dur- 
ing the wet seasons. Second growth or stunted kaffir corn and 



-16 



VETERINARY PATHOLOGY. 



sorghum plants are more likely to be injurious than first 
growth or well developed plants. 

Poisonous plants usually have some noxious properties as 
odor, taste, or appearance that protects them from consump- 
tion by animals. Poisoning usually occurs in animals that are 
hungry or are not accustomed to the location, or at least are 
not familiar with the plants that abound there. Animals in 
districts where poisonous plants are found are usually familiar 
with the disagreeable properties of them and let them alone or 








Fig. 16. — Red Buckeye (Aesculus Pavia). 



the animals may become accustomed to the injurious principles 
of the plant, that is, develop a tolerance similar to immunity to 
infective diseases. 

In their vital activities microphytes (bacteria, yeast and 
moulds) and micrbzoa (protozoa) produce chemic substances 
that are extremely poisonous to animals. Thus saphrophytic 
bacteria produce ptomains in putrefying flesh. Fermented, musty 
or mouldy hay contains injurious substances that produce indi- 
gestion in the horse and ox. The specific products of micropara- 



GENERAL CONSIDERATION OF DISEASE. 



47 



sites will be discussed under the topic of vital or infective 
causes of disease. 

Bees, wasps, scorpions, ants and other animal organisms 
liberate poisonous chemic substances (zootoxins) which, when 
introduced into the animal body cause marked disturbances. 

Poisonous snakes secrete and liberate injurious chemic sub- 







A 




\^* 



'"S'- 

















y 






-^ 








Fig. 17. — Loco (Astragalus Mollissimus"). 



stances. The poisonous principle, zootoxin or venom is pro- 
duced bv glandular tissue, and is liberated through canals or 
grooves in their fangs. The exact chemic composition of venom 
has not been determined but is not the same in the different 
venomous snakes. Xoguchi has classified the principle action 
of venom as follows : — 



48 VETERINARY PATHOLOGY. 

1. Instantaneous production of thrombi. Crotalus (rattle- 
snake). 

2. Neurotoxic action. (Cobra.) 

3. Produce capillary ruptures and hemorrhage. Crotalus 
(rattlesnake). 

4. Produce hemolysis. Crotalus (rattlesnake). 

5. Produce general cytolysis. Crotalus (rattlesnake). 

and viper berus (adder). 

The following is the toxicity estimate of venom per kilo- 
gram body weight : — 

Cobra venom .00009 gram lethal dose for horse intravenously. 

Cobra venom .0005 gram lethal dose for dog subcutanously. 

Rattlesnake .005 gram lethal dose for rabbit subcutanously. 

Viper .0001 gram lethal dose for rabbit intravenously. 

Retrograde metamorphosis in the tissues of the animal body 
frequently results in the production of leucomains which when 
absorbed are extremely poisonous and cause marked disturb- 
ances. Over action of muscular tissue may cause the produc- 
tion of leucomains, thus horses that are overworked, although 
their food and water are first-class and their digestion is good, 
are occasionally affected with a severe diarrhoea caused by the 
action of leucomains. 

Parasitic or Infectious. During the last quarter of a century 
pathology has received an impulse by the knowledge of micropar- 
asites acquired during this time. Although parasitism has been 
known since the dawn of the 19th century the importance of 
• microparasites has been recognized only since bacteriology be- 
came a science. 

Parasitism is an evolutionary condition. It is the result of a 
long continued struggle, and the survival of the fittest, during 
which there is a necessary adaptation to constantly changing en- 
vironmental conditions. Parasitic causes of disease include rep- 
resentatives of both the plant and animal kingdom. Parasitic 
plants (Phytoparasites) are practically all microscopic in size 
and are termed microphytes. Pathogenic plants are all fungi 
and the following scheme gives their position in the plant king- 
dom : 

VEGETABLE PARASITES. 

KINGDOM BRANCH CLASS ORDER FAMILY GENUS SPECIES 

1. Plant Thallophyta Hyphomycetos Mucidineae Oospora Porrigines 

(Achorion 
•choenleini) 

2. Plant Thallophyta Hyphimycetes Plecascineae Aspergillaceae AsperpHlus Fumigatus 
S. Plant Thallophyta Hyphomycetes Plecascineae Afpergillaceae Aspergillus Niger 

4. Plant Thallophyta Ascomycetes Protoascintae Saccharomycetaceae Sacoharomyces Farciminosus 

5. Plant Thallophyta Schizoinycetes .., • Aotinomycea Bovls 

6. Plant Thallophyta Schizomyc«tes ., , Bacterium Tuberculosis, etc 



GENERAL CONSIDERATION OF DISEASE. 



49 



Hyphomycetes (Moulds). 

Hyphomycetes or moulds are non-chlorophyllic plants. Struc- 
turally they are composed of mycelial threads from which up- 
right reproductive organs may be formed. They are usually 
multicellular and reproduce by spores. They require preformed 
foods and thrive best in the absence of light. 

Oospora p'orrigines (Achorion Schoenleini) is the organism 
that causes favus. These organisms have mycelia with hyphae, 
the latter may be branched and terminate in bulbous ends. The 
mycelium is later converted into oval spore-like bodies. Favus 
is occasionally observed in dogs and cats, more rarely in horses 
and fowls. The disease is characterized by dry scales which 
are brown, yellow or even white upon the surface and vary 
from white to sulphur yellow in their deeper layers. The areas 
involved are usually not more than ^ or ^ inch in diameter, 
and are usually devoid of hair. The lesion may occur on the 
head, especially on the forehead, cheeks or ears, and on the 
abdomen, or outer surface of the hind legs. 

Sporotrichmm Audoiiini (Trichophyton Tonsurans) is the 
fungus that causes ring-worm (tinea tonsurans). This fungus is 




Fig. 18. — Trichophyton Tonsurans, showing- mycelium and spore like bodies. 



50 



VETERINARY PATHOLOGY. 



found in the lesion and is probably strictly parasitic. Structurally 
it is composed of a simple or branched mycelium which may 
become broken up as a thread of ovoid spores. The spores may 
also appear in groups in the hair follicles. The disease becomes 
evident because of the presence of small circular hairless patches 
which are covered by grayish crusts or scales. As the disease 
progresses the central portion of the lesion becomes normal and 
the peripheral tissue becomes involved. This condition has 
been observed in the horse and ox ; other domestic animals 
rarely become affected. 

Aspergillus Fumigatus is responsible for an occasional out- 
break of pulmonary mycosis (Pneumo-mycosis Aspergillosis) 
in birds. This fungus is of common occurrence in nature. 
Structurally the fungus consists of a segmented mycelium 




Aspergillus Fumigatus. 



which may branch dichotomously and from which upright 
stems termed hyphae may originate. These hyphae ma}- be 
segmented and terminate in club-like heads. A tuft of hair- 
like projections (sterigmata) develops from the hypha head and 
on the distal end of each hair there is a spore bearing organ 
(conidium). The entire hypha head with its spore bearing 
organs is included in a capsule the rupture of which is nec- 
essary for the distribution of the spores. The spores of Asper- 
gillus are present in large numbers in hay, straw, barn-yard 



GENERAL CONSIDERATION OF DISEASE. 51 

manure, etc., and they maintain their vitality in the dormant 
state for a considerable length of time. 

The source of infection is contaminated food, water or air. 

The principal lesions are located in the trachea, bronchi, 
lung and air cells of bones. The disease is characterized by a 
fibrinopurulent inflammation of the mucous membranes of the 
trachea and bronchi and abscess formation in the lung. 

Aspergillus Niger is probably responsible for the cause of 
some cases of ear canker in dogs. 

Saccharomyces. (Yeast). 

Saccharomyces are the budding fungi. The classification of 
this group, the yeast plants, is as yet incomplete, their general 
biologic characteristics not being well known. A few varieties, 




SVy" 

Fig. 20. — Yeast (Saccharomyces Farciminosus). 

however, have been studied, one of which, Saccharomyces Cere- 
visiae, is of considerable economic importance to the brewers. 

Yeasts are ovoid or spherical single celled non-chlorophyllic 
plants that reproduce by budding. Structurally the yeast cell 
has a cell body composed of protoplasm and a double cell mem- 
brane the latter composed of condensed protoplasm. The cell 
body may contain vacuoles, granules or foreign substances. 
Reproduction, which is by budding or gemmation, occurs at one 
or both ends of the yeast cell and even in some cases from 
the side of the cell. Budding begins by the appearance of small 
tubercles or buds which develop until a considerable size is 
attained. The daughter cell may remain associated with the 



52 VETERINARY PATHOLOGY.' 

mother cell or it may become detached and then pass through 
a similar cycle. Under certain conditions the yeast plant may 
develop into filamentous threads and in other instances may 
produce spores. 

Saccharomyces was, for a considerable time, associated as 
an etiologic factor in the production of carcinoma. It is prob- 
able that the "carcinoma bodies" (dense refractile oval bodies) 
are yeast cells but it is quite evident that they have no etio- 
logic significance in carcinomata. 

Dermatitis in the human is, in some instances, of a saccharo- 
mycetic origin and no doubt some of the resistant cases of der- 
matitis in domestic animals have a similar cause. 

The principal pathogenic saccharomyces that concerns the 
veterinarian is the Saccharomyces farciminosus, which has 
been described by Rivolta as the Cryptococcus farciminosus. 
This yeast is the cause of epizootic lymphangitis, a disease 
which affects equines and primarily involves the cutaneous 
lymphoid tissue. The disease is prevalent or has prevailed in 
many localities in the United States, and in the Phillipines, 
as well as, in India, Japan, China, South Africa, England and 
Ireland. The principal lesions are located in the lymphoid 
tissue which becomes tumefied and inflamed and in which the 
lymph sinuses are found to be engorged with coagulated lymph 
and pus. The lymphoid tissue later undergoes central liquefying 
necrosis and this is followed by the formation of pustules or 
ulcers. After the discharge of the pus the ulcer gradually heals 
and the related tissue becomes indurated. In a few cases 
lesions have been observed in the liver and spleen. 

Two other pathogenic fungi that have not been satisfactorily 
classified are the Actinomyces Bovis and the Botryomyces 
Ascoformans. These are the causative agent of Actinomycosis 
and Botryomycosis respectively. These micro-organisms as 
well as the diseases they produce will be discussed later. 

Schizomycetes. (Bacteria). 

As will be noted by the foregoing scheme, bacteria are 
classed among the lowest groups of plants. Each bacterium is 
a single cell and contains no chlorophyll. 

The science of bacteriology is of recent development, because 
early investigators were compelled to use comparatively crude 
microscopes and because they were not familiar with the condi- 
tions required for bacterial growth. The development of bacter- 
iology was coincident with the discussion pro and con of the 
theory of "spontaneous generation." This theory was disproved 



GENER.\L CONSIDERATION OF DISEASE. 53 

by Pasteur about 1865, whose classical experiments also aided in 
establishing bacteriology as a science. (It is possible that bio- 



•. • ••, 







» • i • •• ^ •• 

1 Z 3 4 a 

Figr. 21. — Showing- different forms of Cocci. 

1. Micrococcus. 4. Tetrads. 

2. Streptoccus. 5. Sarcina. 

3. Diplococcus. 

chemists may produce life, (animate objects), by synthesis of 
inanimate substances which will only represent the achieve- 
ments of ultratechnical scientists and will not signify that spon- 
taneous generation occurs in nature). Thirty or forty years 
ago the study of bacteria was looked upon as a fad by the 
majority of the people. However, the practical application of 
bacteriologic knowledge in medicine, sanitation, the ivarious 
arts and agriculture, has caused bacteriology^ to assume its 
present important position as one of the principal biologic 
sciences. 




//.-. 



Fig. 22. — Various forms of Bacilli. 

Bacteria are found everywhere that animals or higher plants 
have groAvn. They are practically omnipresent. 



*v 



i^ ' N-^Jx 'h 



Fig- 23. — Various forms of Spirilla, 

Bacteria are single celled plants, each individual possessing a 
cell body and a cell membrane. The cell body is principally 
composed of protoplasm, which may be homogeneous or granular. 
In some instances non-protoplasmic particles may be present. 
Chromatin, the essential nuclear material, is regularly distrib- 
uted throughout the entire cell body and no doubt functions 
the same as a nucleus. Granules that are intensely stained 
with methylene blue occur in the body of some bacteria, but 
their significance is not known. The cell bodies of some bacteria 
contain starch granules while those of others contain sulphur 



54 VETERINARY PATHOLOGY. 

granules. The cell membrane is of a protoplasmic nature and 
is probably formed by condensation of the p\ otoplasmic eel- 
body, whereas cellulose constitutes the cell mwmbrane of the 
cells of higher plants. Some species possess orj^ans of locomo- 
tion called flagella, which are delicate protoplasmic projec- 



m-^ 





Fig. 24. — Flagellate bacteria of various forma 




tions of the cell body or cell membrane. Some bacteria, per- 
haps all, possess a capsule which appears as a gelatinous sub- 
stance and is probably derived from the cell membrane. The 
cell body is the essential structure and presides over metabol- 
ism, reproduction and practically all other functions. Circu- 
latory, nervous and excretory organs are obviously not required 
in such simple forms of life. The cell membrane protects the 
cell body. 

Fig. 25. — Bacteria, showing capsule. 

Bacteria are very small, one eight millionth part of a cubic 
inch has been estimated as the least mass capable of being de- 
tected with the naked human eye. This space may contain 
about 2,000,000 bacteria. The dimensions of bacteria are ex- 
pressed in the term micron which is the unit of microscopical 
measurement. (A micron is 1/25,000 of an inch and is desig- 
nated bv the Greek letter "Mu".) The Bacterium tuberculosis 
averages about 2.5 microns in length and about .5 microns in 
width, i. e., 1,000 tuberculosis organisms placed end to end 
would make one inch in length or it would take 50,000 of these 
bacteria placed side l)y side to make a linear inch. Some spher- 



CJENERAL CONSIDERATION OF DISEASE. 55 

ical bacteria are less than one micron in diameter, e. g., the 
pyogenic staphylococci average .8 of a micron in diameter. 
Different individuals of the sanie species may vary considerably 
in size, thus the Bacterium anthracis may varv from four to 
ten microns in length. Some diseases are probably the result 
•of infection with micro-organisms that are so small they can- 
not be detected by the use of present day microscopes and they 
also pass through the best known germ-proof filters. These in- 
fectious agents are designated as invisible or ultra-microscopic 
and may be present in a "filterable virus." 

Morphologically bacteria are very simple. Three principal 
types of bacteria are recognized according to their form, viz: 
the rod shaped (Bacteria), spherical (Cocci), and the spirals, 
(Spirilla). Another type, characterized by branching forms,, 
(Chlamy do-bacteria), has a few representatives but their classi- 
fication as bacteria has been questioned. The representatives 
of each of the three principal groups. Bacteria, Cocci and 
Spirilla, are constant in their morphology so long as the environ* 
ments remain the same, i. e., the progeny of bacilli are bacilli, 
€tc. Again, each individual is constant in its form, increase in 
size being the only change that occurs. Frequently, however, 
unfavorable conditions may cause pleomorphism among indi- 
vidual organisms. 

Perhaps the best accepted morphologic classification of bac- 
teria is as follows : — 

1. Coccaceae, spherical shaped bacteria. 

2. Bacteriaceae, rod or cylindrical shaped bacteria. 

3. Spirillaceae, spiral shaped bacteria. 

4. Chlamydo-bacteriaceae, branching or irregular forms t^i 
bacteria. 

According to their biologic characteristics, bacteria may be 
classified as follows : — 

Aerobic or anaerobic. 

Chromogenic or non-chromogenic. 

Zymogenic or non-zymogenic. 

Saprogenic or non-saprogenic. 

Photogenic or non-photogenic. 

Thermogenic or non-thermogenic. 

Saphrophytic or non-saphrophytic. 

Parasitic or non-parasitic. 

Pathogenic or non-pathogenic. 

Pyogenic or non-pyogenic, etc. 

Bacteria, like other living things, grow and reproduce under 
favorable conditions. They grow until they attain a certain size 



VETERINARY PATHOLOGY. 

then they divide, i. e., a cell divides into two equal halves, each 
half representing an individual bacterium which in turn "^rows 
and ultimately divides into two equal halves, etc., thus bacteria 
grow and multiply. The rate of growth and division is com- 
paratively rapid. The Bacillus subtilis, under favorable con- 
ditions may pass through the life cycles incident to attaining 
its growth and dividing, thus doubling in number, every 30 min- 
utes. Barber has found that Bacillus coli communis, under 
optimum conditions may divide by fission, in seventeen min- 
utes. Beginning with one bacterium, it has been estimated that 
if division occurred once per hour and continued for three days, 
the progeny would weigh 7,4T7 tons. Some other cells, notably 
the undifferentiated cell in the animal embryo, may divide as 
rapidly as bacteria, but they do not become developed, and so 
far as known, there are no other cells that complete the entire 
cycle of growth and reproduction in so short a time. This 
method of reproduction is called fission. Fission occurs in the 
three principal forms of bacteria. Among the Bacteriaceae and 
Spirallaceae, the division takes place in the transverse diameter, 
while the Coccaceae may divide in one, two or three planes. 




Fig. 26. — Bacteria, showing fission. 



Bacteria grow and divide by fission as long as favorable 
conditions are supplied. When the environments are unfavor- 
able the organisms cease growing and do not increase in num- 
ber. Some species produce spores when conditions become 
unfavorable for further growth and fission. Bacterial spores, 
generallv characterized by being small, highly refractive oval 
shaped bodies, are more condensed than the original cell body 
protoplasm. Spore formation is first indicated by the appearance 



GENERAL CONSIDERATION OF DISEASE. 



0/ 



of small granules in the protoplasm of the parent cell. These 
granules collect and ultimately coalesce thus forming the spore. 
The spore may form in the center of the bacterium or near one 
end. After the spore is formed the remainder of the bacterial 
body becomes disintegrated. Spores are much more resistant 
to external injurious influences than are bacteria. The resist- 
ance of spores is due to the fact that they contain less water 
than bacteria, moreover thev enjoy the protection of a thick 
covering or cell wall. Spores are inactive, i. e., they remain dor- 
mant until placed in favorable media and under favorable con- 
ditions when thev germinate and develop as the vegetative 
form. One bacterium produces only one spore which in turn 
produces only one bacterium and hence spore formation is not 
a means of multiplication, but is rather a natural means of pre- 
servation or continuation of the species. Those species of 
bacteria in which no spores are formed usually have a greater 
resistance to injurious influences than do the vegetative forms 
of the species which are capable of producing spores. 




Fig-. 27. — Showing spore formation. 



Bacterial food requirements are quite variable. Some types 
of bacteria require preformed organic compounds and others 
appear to have the power of synthesizing the simplest com- 
pounds and available elements into new compounds upon which 
they subsist. Until recently it was supposed that synthesis was 
confined to chlorophvllaceous plants but some species of bac- 
teria are now known to posess the power of building complex 
compounds from simple materials, e. g.. the nitrifying bacteria. 
Parasitic bacteria and most saprophytic bacteria as a rule 
require preformed organic compounds for their food. Some 



58 VETERINARY PATHOLOGY. 

soil bacteria and many water bacteria appear to live and thrive 
on simple inorganic substances. In fact most bacteria are capable 
of adapting themselves to an inorganic food medium. Food sub- 
stances must be in a dilute form in order that bacteria may 
subsist upon them. This is probably because of the osmotic 
differences of bacteria and their surroundings. Some 
chemic substances, usually considered as destructive to 
bacteria, w^hen sufficiently dilute are food for some organisms, 
thus the Bacillus Pantotropus produces formalin and then uses. 
it for food. It is said that BacillusPantotropus may live and 
thrive in a 1 to 15,000 solution of formalin. Bacteria as a rule 
require food media of neutral or slightly alkaline reaction, (as 
shown by litmus paper) though some grow readily in acid media.. 
While foods are required in small quantities only for each 
bacterium, yet because of their rapid mutiplication and the 
resulting enormous numbers, the quantity of food substances- 
consumed by them becomes of considerable importance. 

Most foods of bacteria like those of animals or higher plants, 
must uindergo modification preparator}^ to assimilation. As 
previously stated, bacteria do not possess a digestive tube 
neither do they have the power of enveloping particles of food 
as do some protozoa. Bacterial digestion is an extracellular 
process, i. e., the bacterium digests food substances that are: 
DUtside of its own body. This process is the same as the 
digestion in higher animals, the digestive tube in the latter- 
being outside of the body tissues. Bacterial digestion is the 
result of activity of ferments produced by the body protoplasm 
and in this respect is comparable with equine digestion which 
is the result of activity of ferments produced by protoplasm 
of the salivary, gastric, pancreatic cells, etc. Some bacterial 
digestive ferments are very similar if not identical to the 
digestive ferments of 'higher animals. 

Digested foods or food substances in solution pass into the 
bacterial body by osmosis. 

Bacterial respiration is a simple process. The exchange of 
gas is probably accomplished by means of the transfusion of 
fluids containing the respiratory gas. Bacteria may vary in their 
oxygen requirement. Aerobic bacteria are those that require 
oxygen as a respiratory gas. Some bacteria will not develop 
in the absence of free ogygen, obligatory aerobes. Although 
it was originally supposed that all forms of life required free 
oxygen this is now known to be an erroneous idea. Thus, the 
anaerobic bacteria require the absence of free oxygen ; and some 
organisms, — obligatory anaerobes — require the absolute absence- 



GENERAL CONSIDERATION OF DISEASE. 59 




Bacterium Anthracis. 



of nncombined oxygen. Other bacteria, facultative aerobes or 
anaerobes, are not so selective in their oxygen requirements, 
e. g., some are capable of immediate adaptation to a medium 
containing free oxygen. It is probable that anaerobic bacteria 
require oxygen as a respiratory gas but the oxygen is obtained 
from oxygen compounds that are decomposed by these bacteria, 
the oxygen probably being consumed while in the nascent state. 

]\Ioisture, temperature and light are other physical condi- 
tions that affect bacterial development. A very few bacteria 
will remain active in substances containing less than twenty 
per cent of water. The optimum condition relative to moisture, 
requires the presence of about 80% of water. This fact is 
observed in the preparation of dried food stuffs and is the 
essential reason whv dessicants favor wound healing or retard 
infection. The temperature range of the various bacteria is 
wide. Some bacteria live and thrive at a temperature near the 
boiling point, others at a freezing temperature. Pathogenic bac- 
teria, in general, require the temperature of their host. The 
chicken has a verv high normal temperature (107° to 108° F.),. 
and this may explain Its immunity to practically all the diseases 
that affect other domestic animals. All' bacteria require the 
absence of light for their best development. Bv adaptation some 
have become capable of growing and thriving In daylight. 

The effects of bacterial growth and the products evolved 
during bacterial growth vary according to the microorganism 
in question and Its environment. Heat and light are two forms 
of energy produced by bacterial activity. The heating observed 



60 



VETERINARY PATHOLOGY. 




rig. 29. — Bacillus Tetani. 



in manure piles, alfalfa, hay and various grains in the stack is 
thought to be the result of bacterial action. In the above sub- 
stances, the contained moisture favors the growth of bacteria and 
the growth of zymogenic bacteria is always dependent upon 
chemic changes in which complex compounds are reduced to 
simpler ones. Such chemical changes are accompanied by the 
evolution of heat. In all fermentation, in which the substances 
acted upon are converted into simple compounds, heat is liber- 
ated. Light or phosphorescence may be produced by bacteria. 
The phosphorescence of decayed wood, ocean water, flesh, etc., 
may accompany the growth of light producing bacteria. Light is 
a form of energy and bacterial light or phosphorescence is the 
result of the conversion of some other form of energy usually 
kinetic energy, into ether vibrations or light. The production 
of heat and light are of little importance in comparison with 
other bacterial products and activities. 

Pigments of various kinds are produced by several different 
species of bacteria. These pigments may be an excretion or a 
secretion or thev ma}^ possibly represent synthetic extnicellular 
products or enzymotic by-products. The importance of bac- 
terial pigments is largelv confined to the discolorizatiou of food 
substances. Thus the Micrococcus roseus. Bacillus pnidigiosus, 
and Bacillus erythrogenes, produce a red pigment in milk. The 
red pigment in the milk is sometimes mistaken for bloody milk. 



GENERAL CONSIDERATION OF DISEASE. 61 

Other bacteria produce a variety of pigmentation in food 
substances. These pigments are variable in composition and 
solubility. Generally speaking the bacterial pigments are not 
injurious when consumed. Practically all pigment producing 
bacteria are aerobic. 

The principal action of most bacteria is the result of the 
activity of ferments or enzyms produced by the bacterial pro- 
toplasm. Some of these bacterial ferments may produce their 
specific activity while inside the bacterial body, others 
bring about specific changes after being secreted and eliminated 
from the bacterial bod3\ The end products resulting from 
the activity of bacterial enzyms or ferments are variable and 
depend upon the specific enzym or ferment also on the compo- 
sition of the substances acted upon. Acids or alkalies represent 
the end products of many of the bacterial decompositions. 
Carbohydrates are usually converted ultimately into an acid, 
carbon dioxide and water. Protein substances may be con- 
verted into carbon dioxide, water and ammonia by the activity 
of Bacillus pyocyaneus. 

Putrefaction is a bacterial decomposition of nitrogenous 
substances and occurs in the absence of air. The end products 
of putrefaction are extremely variable; hydrogen, carbon 
dioxide, nitrogen^ hydrogen sulphid, and ammonia, are some 
of the common gases that escape from a putrefying carcass ; 
amido compounds, pepton, skatol and indol represent aromatic 
compounds ; ptomains probably represent one of the most im- 
portant putrefactive products. Ptomains are basic chemic 
substances produced by decomposition of nitrogenous com- 
pounds. They are usually formed outside the body, although 
they may be formed by putrefaction of the contents of the 
intestine. Ptomain poisoning is usually the result of consump- 
tion of foods contaminated with ptomains although it mav 
result from the absorption of ptomains formed within the in- 
testine. Sufficient ptomains may also be absorbed from 
necrotic tissue to produce injurious effects. 

The chemic substances produced by pathogenic bacteria are 
probably of more importance than any other bacterial com- 
pounds. Although thev have been extensively studied the com- 
position of most of these compounds is still unknown. Three 
groups of pathogenic bacterial products deserve mention ,they 
are (1) bacterial toxins, (2) endotoxins and (3) bacterial pro- 
teids. 

1. Bacterial toxins are soluble, synthetical, poisonous, 
chemic substances elaborated by the bacterial protoplasm and 



62 VETERINARY PATHOLOGY. 

liberated into the surrounding media. The chemic composi- 
tion of bacterial toxins is unknown. They are very similar in 
many respects to enzyms. They are specific, i. e., a given 
organism always produces a definite toxin. According to 
Ehrlich bacterial toxins are composed of two combining 
groups, one the haptophore which combines with the receptors 
of the animal cells and form a medium through which the other 
group, toxophore, acts. They are the principal product in 
some infection, e. g. tetanus. (Infection is the invasion into a 
living body of pathogenic micro-parasites, and the sum total 
of the disturbance produced by their presence in the body). 
During infection the body attempts to neutralize bacterial 
toxins by the production of a substance termed an antitoxin. 

2. Endotoxins are poisonous chemic products formed and 
retained within the bacterial body. They become liberated only 
when the bacteria are destroyed and disintegrated. Although 
the chemistry of endotoxins is not known, they are probably 
constant in composition and produce specific symptoms in in- 
fected animals. The animal body does not produce antibodies 
that neutralize endotoxins, but opsonins, bactericidal sub- 
stances and agglutinins are produced in the tissues of animals- 
immunized to endotoxins. Endotoxins are the principal in- 
jurious substances produced by pyogenic Cocci, Bacterium 
Tuberculosis, the organisms causing glanders, pneumonia, and 
other specific infections. 

3, Bacterial proteids are insoluble nitrogenous constit- 
uents of the bacteria cell protoplasm. They are not well under- 
stood. (See insert No. 2.) 

ANIMAL PARASITES. 

The animal parasites, capable of producing disease in an- 
imals, are quite numerous and represent the following branches, 
of the animal kingdom : — protozoa, helminthes, and arthropoda. 




Fig. 30. — Piroplannia Bigeininum in the rod bl'>ocl corpuscles. 



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GENERAL CONSIDERATION OF DISEASE. 



6^ 



Protozoa. 

Protozoa are microscopic single celled animals. They are 
very simple in structure, being composed of a mass of proto- 
plasm with or without a cell membrane. The cell membrane, 
when present, consists of concentrated protoplasm. The pro- 
tozoa having a cell membrane are constant in shape, as the Try- 
panosoma Evansi, and those not possessing a cell membrane 
vary in shape from a sphere to an irregular flat mass and are 
capable of changing their shape whenever occasion demands. 
Protozoa are larger than bacteria. 







Fig:. SI. — Trypanosoma Evansi in a bloodsmear from a horse affected with surra. 

Protozoa require food similar to the foods of higher animals. 
Particles of food are inclosed or incorporated by them prepara- 
tory to digestion. Digestion is accomplished by means of fer- 
ments elaborated and secreted by the protozoa. The digested 
foods pass by osmosis into the protozoa, the undigested por- 
tion being extruded by rearrangement of the cell protoplasm. 
Respiration takes place by exchange of gases through the 
surface protoplasm of the protozoa. They reproduce by fission, 
budding, conjugation or sporulation. 

Protozoa are universally distributed. They all require con- 
siderable moisture. In fact most of them live either in fresh or 
salt water. A few only are parasitic. 

The specific action of pathogenic protozoa in the produc- 
tion of disease is not understood. Some may have a mechanical 
eifect only out the evidence concerning others indicates that 
most of them produce an injurious chemic substance. 

Helminthes. 

This branch of the animal kingdom contains many species 
that are parasitic. Structural, animal parasites are much simpler 



64 



VETERINARY PATHOLOGY. 




F'ig. 3 2. — Sart'ocystis Miescheri. Drawing made with Camera lucida. 

1. Cross secti>)n sarcocyst, muscle cell enclosing sarcocyst ruptured. 

2. Cross section of heart muscle cell. 

3. Fibrous connective tissue. 



than the closely related nonparasitic animals. The simplicity of 
parasites is a result of adaptation to environments in which es- 
sential structures of the nonparasitic type, useless to the para- 
sitic type, atrophy because of disuse. The parasitic helmintlies 
are of the simplest structure, their nervous, digestive and respi- 
ratory systems being" very rudimentary. 

Their food is obtained from their host. Some animal para- 
sites, as the tapeworm (Taenia) absorb digested food stuff frc^n 
the intestine of their host, others subsist upon the host's blood, 
(Uncinaria), and still others consume tissue juices and lymph, 
(Trichina spiralis). The reproduction of helminthes is accom- 



BRANCH 

PROTOZOA, 

Unicellular animal organ- 
isms, asexual. reproduce 
by fission, sporulation. or 
budding-. 



OEDER 

SPOHOZOA, 

Reproduce by sporulation, 

no flagella, no cillia. 



INFUSORIA, 

Possess cilia or flagella, 

reproduce by fission and 

budding. 



CLASS 

COCCIDIA. 



SARCOSPORIDIA. 



FLAGELLATA. 



HTPOTRICHA. 



ANNULATA, 

Specialized worms com- 
posed of ring like sege- 
ments, simple head and 
eyes, usually evergible 
dentated pharynx, straight 
alimentary canal, well de- 
veloped nervous system. 



HIRUNDINEA, 
Slightly flattened on dor- 
feal and ventral surface, 
sucker at each end. 



GNATHOBDELLA. 



INSERT III. 



AjMTLY 

50R0SPERMIDAE. 



GENUS SPECIES 

Coccidium oviforme 
Coccidium cunicull 
Coccidium avium 



HOST 



PART rNFESTED 



Rabbits, G. pigs and man Liver and intestine. 

Rabbit. Lieberkuhn's glands and intestine. 

Fowls. Liver and intestine 



.RCOSPORIDAE. 



Sarcocystis Miescheri 
Sarcocystis tenella 
Balbiania gigantea 



Pig. Muscles. 

Horse, ox, sheep, and pig. Muscles. 
Ox, sheep and dog. Connective tissue. 



^RCOMONIDAE. 



Lamblia intestinalis 
Monocercomonas hepatlca 



Trypanosoma equiperdum. 
Trypanosoma Evansi. 
Trypanosoma equinum. 
lYPANOSOMATIDAE. Trypanosoma Brucei. 



ilATHOBDELLIDEA, Hirudo medicinalls. 
' Hirudo troctina. 

Hirudo decora. 

Hirudo Tagala. 

Haemopis sangulsuga. 



Sheep and dog. 
Pigeons. 


Intestine 
Liver. 


Horse. 
Horse. 
Horse. 
Horse. 




Blood. 
Blood. 
Blood, 
Blood. 


Man and 
Man and 
Man and 


horse, 
horse, 
horse. 


Skin. 
Skin. 
Skin. 



Man and animals. 
Horse. 



Anterior respiratory tract and intes- 
tine. 



GENERAL CONSIDERATION OF DISEASE. 



65 




Fig. 33 




p, Sj 



Fig. 33c. 



Fig. 33d. 



Fig. 33. — Taenia 3Iarginata. After Niles. 



a. Shows segments. 



b, c. 
d. 



Head latteral view. 
Head anterior vieAV. 



plished by means of ova, or by the production of living larvae. 
The life history or cycle of helminthes is very interesting. In 
some cases the organism is parasitic in diiTerent animals during 
the different stages of its life cycle ; for instance the Taenia eras- 



66 



VETERINARY PATHOLOGY. 






Fig. 34. — Taenia Carina. After Railliet & Leuckart. 

a. Adult tapeworm. c. Cystic form. 

b. Head of same enlarged. 









4- 



■':■<■■ .-.■■I'i 




•^iiii^r' 

















Fig. 35. — Taenia Eehinoeoccus. Niles &- Neumiu 
a. Adult tapeworm. After Nouman. b. Part oC hog's liver showing cystic form. 



BRANCH CLASS 



OBDEB 



FAMILY 




PLATYHEaL-MINTHES, 
Flat worms, nearly 
hermaphodites. 



all 



CESTODA, 

Ribbon shaped, segment- 
have no fixation apparatus 
have no digestion apparatus 
on head. Adult lives in In- 
testines. 



NEMATHELMINTHES, 
Round worms, nonseg- 
mented, sexes separate. 



TRBMATODA, 
F;at worms, nonsegment- 
ed, have digestive canal, 
no anus, have one or two 
suckers on ventral surface. 



ACANTHOCEPHAL.A. 
Slender worms, complete 
digestive canal, are found 
in all tissues of domestic 
animals except bone. 



TABNIIDAE, 

Head always has four 
suckers between which is 
found a depression or a 
proboscis. Segments usu- 
ally have their gential op- 
enings on margin. 



NEMATODA, 

Slender worms, complete 
digestive canal, are found 
in all tissues of domestic 
animals except bone. 



STRONGTLIDAE, 

Body cylindroid, mouth 

either nude, armed or 

papillated, oseophagus 

large. 



TRICHOTRACHELIDAE, 
Body slender in anterior 
portioh, enlarged poster- 
iorly for containing intes- 
tine, mouth nude, anus 
terminal, all live in intes- 
tine. 



FILARIDAE, 

Long thread like body, 
mouth or triangular , oeso- 
phagus small. 



GNATHOSTOMIDAE, 
Head distinct, oviparous. 



BOTHRIOCEPHALIDAE, 
Found mostly in fishes. 



DISTOMIDAE, 

All have two suckers, an 

anterior and ventral. 



ECHINORYNCHIDAE, 
Found in digestive canal 
of vertebrates. 

I ASCARIDAE, 
Large firm body, resemble 
earth worms, mouth is 
surrounded by three lips. 
Usually found in small in- 
testine. 



OXYURIDAE, 
Cylindroid body, tail 

pointed, mouth nude, 
stomach large. 



SPECIES 



HOST 



PART INFESTED 



laginatta 








Man 


'yst; Cysticercus 


cellulosae, 


of 


pig.) 


solium 








Man 


yst ; Cysticercus 


bovis. 


of 


ox) 




erfollata 








Horse 


lamiliana 








Horse 


Ucata 








Horse 


enticulata 








Ox 


xpansa 








Ox and 


mbriata 








Slie«>p 



sheep 



Intestine 
Intestine 
Intestine 
Intestine 
Intestine 
Intestine 
Intestine 
Duodenum and ffall duet 

Intestine 



-larglnata Dog Small intestine 

Cysticercus tenuicollis of rumin ants.) 

;'oenurus Dog-, wolf and fox Small intestine 

yst: Coenurus cerebralis in spinal coid and brain of sheep.) 
chinococcus Dog and wolf Small intestins 

■St; Echinococcus polymorphous, of herbivora and omnivora ) 
?icumerina Dog 

St; (1) Crvptocystis trichodectis of Trichodectes latus.) 
'st; (2) Cryptocystis pulecides of Pulex serratlceps. ) 



!3phalus latus 



Man, dog, cat 



Intestine 



C hepatlcum 
: lanceolatum 

C Americanum 
/sma cervi 
mus Westermanii 



Herbivora and omnivora Gall ducts 
Sheep, ox, goat, pig, ass, Gall duets 

dog 
Sheep and ox Liver 

Ruminants Rumen 

Man, dog, pig and cat Lungs 



nynchus gigas 



Pig 



Small intestine 



Anegalocephalus 
bovis 

')vis 
ailla 

narginata 
i^nystax 



Solipeds 

Ox 

Sheep 

Pig 

Dog 

Cat 



Small Intestine 

Intestine 
Intestine 
Intestine 
Intestine 
Intestine 



Ocurvula 
Qmastigodes 



Horse 
Horse 



Posterior bowel 
Posterior bowel 



jas Arnfeldi 
-lis micrurus 
dis pulmonaris 
ius filaria 
r'us rufescens 
-us paradoxus 
>us Osteragi 
iis contortus 
^s filicollis 
^us gigas 
^is vasorum 
-)ma equinum 
^ma tetracanthum 
;ima hypostomum 
Is trachealis 
jirus dentatus 
la trigonocephala 
Ja cernua 
a radiatus 



Solipeds 

Bovines 

Calf 

Sheep, goat, camel, deer 

SheeT\, goat and deer 

Pig 

Ox 

Sheep, goat 

Sheep and goat 

Horse, ox, dog and man 

Dog 

Horse, ox, dog and man 

Solipeds 

Sheep and goat 

Birds and chickens 

Pig 

Dog and fox 

Sheep and goat 

Bovines 



Bronchi and lungs 

Bronchi and lungs 

Bronchi 

Bronchi and lungs 

Bronchi 

Bronchi 

Abomasum 

Abomasum and duodenum 

Small intestine and abomasum 

Kidneys and arinary organs 

Heart 

Intestine 

Large intestine 

Large intestine 

rp ■!» ja C Vl G 3* 

Region of kidney and liver 
Small intestine 
Small intestine 
Small intestine 



jPhalus affinis 
jphalus crenatus 

iphalus depressiusculus 
spiralis 



Ox, sheep and goat 

Pig 

Dog 

Pig 



Caecum 

Large intestine 

Caecum 

Muscles 



1)apillosa 

oervina 

mmitis 

ra megastoma 
ra microstoma 
ra reticulata 

ra scutata 

ra sanguinolenta 



Horse 

Ox and deer 

Dog 

Horse 
Horse 
Horse 

Ox, sheep and goat 
Dog 



Peritoneal and plural cavities 

Peritoneum 

Right heart and pulmonary arter- 
ies 

Right stomach 

Stomach 

Flexor tendons asd cervical liga- 
ments 

Oesophageal wall 

Tumors of stomach, gullet and 
aorta 



itomum cheiracanthus 



Pig, dog and cat 



Gastric mucosa 



GENERAL CONSIDERATIOX OF DISEASE. 



t / 



a i 




Fiy. 36. — Taenia Solium. 

0.. b. Adult worm. 
c. Head of same enlarged. 




Fig. 36 c. 




Fig. 37a. 




Fig-. 37b. 

Fig. 37. — Strougylus Miorurus, after Railliet. 

a. Male and female. 

b. Caudal extremity of male. 



68 



VETERINARY PATHOLOGY. 




Fig. 38. — Strongrylus Paradoxus, after Railliet. 

a. Adult male and female. 

b. Caudal extremity of female. 

c. Caudal extremity of male. 





a. Adult male. 



Fig. 30a. and b. 

Fig. 3 tic. 

b. Adult female. c. Cephalic extremity enlarged. 

Fig. 3!). Filaria Papillosa. after Neuman. 



GENERAL CONSIDERATION OF DISEASE. 



69 




^ ^ai 




Fig. 40. — Oxyuris Currula, after Niles. 

.Adult worm. ?. Caudal. 

Cephalic extremity. 



sicollis Inhabits the liver of the rat during- its cystic stage and 
the intestine of the cat during the adult stage. 

Helminthes produce injury to their host by consuming food, 
by sucking blood and by liberating injurious chemic substances. 

Arthropoda. 

This branch includes many parasitic representatives, as flies 
and mosquitoes (diptera), fleas (siphonaptera) lice (hemip- 
tera), itch mites and ticks (acarina). The entire order, siphon- 
aptera and hemiptera, most of the order acarina, and many rep- 
resentatives of the order diptera are parasitic. Of the parasitic 
arthropoda some are temporary and some are permanent para- 
sites, and with one or two exceptions they are all external para- 
sites. 

The structural peculiarities that differentiate arthropoda from 



70 



VETERINARY PATHOLOGY 




Fi? 



. 41 — Synganius Traohealis, 

after Railliet. 
Adult worm natural siae. 
Male attached to female 

enlarged. 
Female enlarged. 




Fig. 42. — Selerostoma Hypostomum, 

after Railliet. 

a. Cephalic extremity enlarged. 

b. -A-dult female. 
0. Adult male. 




Fig. 43. — Triehoceplialiis Deprewsiusculll8 

of a Dog, after Railliet. 



the other branches of the animal kingdom are their jointed ap- 
pendages, segmented body, and bilateral symmetry. 

The parasitic arthropoda ol)tain their food from their hosts. 
Some of them consume epidermal scales and hair, e. g., the 



BRANCH 



CLASS 



ORDER 



FAMILY 







bo 


H 




§ 


0^ 




;« 
t- 


U 




cd 


CO 




CO 


Z 




to 






d 




*«! 






Q 


tu 




O 


p. 
e3 




i 


•J 




H 


C 




» 


O 




< 


•r-5 



INSBCTA (HEXAPODA), 

Air breathers, when adult 
have three pairs of legs, 
and distinct head, thorax 
and abdomen. 



DIPTERA 

Have two wings, two hal- 
teres, sucking mouth parts, 
and complete metamor- 
phosis, includes flies and 
mosquitoes. 



HEMIPTERA 

Wings often absent, when 
present one pair thick and 
one pair thin. ( Suclkjng 
mouth parts, incomplete 
metamorphosis, and include 
the blood sucking lice. 



MALLOPHAGA 
Wingles lice with sucking 
mouth parts, and incom- 
plete metamorphosis. 



SIPHONAPTERA 
Wingless fleas with suck- 
ing mouth parts, and com- 
plete metamorphosis. 



ARACHNIDA 

Air breathers w^ith caphal- 
othorax and abdomen, 
have when adult four 
pairs of legs. Those here 
included are oviparous. 



ACARINA 

Usually short thick, non- 
articulated bodies, possess 
camerostoma, larva usual- 
ly hexapodal, sexes sepa- 
rate. 



LINGUATULIDA. 
Internal parasite, elongat- 
ed, vermiform, annulated 



MUSCIDAE 

Have soft probosis adapt- 
ed for suction, styJ.et of an- 
tennae plumose to the end. 



TABANIDAE 

Broad and slightly flat- 
tened body, large head, 
muscular wings, larva car 
nivarous, are oviparous. 

STOMOXIDAB 

Closely resembles the mus- 
cidae. 

SIMULIIDAB 

Thick body, bulging tho- 
rax, iegs strong. 

HIPPOBOSCIDAE 

Plat body, head notched 

into thorax, legs strong, 

pupiparous. 

OESTRIADAE 

Body usually hairy, large 

wingi, proboscis very small, 

oviparous. 

CULICIDAE 

Have long slendor abdo- 
men, wings fringed with 
hairs, antennae plumose in 
males, oviparous. 

PEDICULIDAE 
Blood suckers, proboscis 
formed of upper and lower 
lips and armed with small 
spines, contains protrusile 
tube or sucker, oviparous. 

RISCINIDAE 

Not blood suckers, have 
long masticatory apparatus 
with w^hich they eat epi- 
dermic j<»roductions, ovi- 
parous. 

PULCIDAE 

Very agile, brown oval 
bodies, compressed latter- 
ly, biting mouth parts in 
larval stage. 



IXODIDAE 

Large globular blood-suck- 
ers, oviparous, have undi- 
vided hypostome. 



GAMASIDAE 

Rostrum arranged for 
pricking or sucking, have 
no eyes. 

TROMBIDIIDAE 

Soft, hairy, bright colored, 

rostrom a conical sucker. 



SARCOPTIDAE 
Smallest of the acarlna, 
body soft, white or red- 
dish, eyes absent, ovipar- 
ous or ovoviviparous. 



DEMODECIDAE 
Very small, vermiform, 
hairless, cephalothorax and 
abdomen distinct, legs 
short, oviparous. 

LINGUATULIDAE 
Body segmented, com- 
pressed dorso-ventrallj'. 
crenelated. 



rs SPECIES 

. domestica 
,, vomitorla 
'>haga carnaria 
xys calcitrans 
tobia serrata 
jomyia macellarla 



HOST 

Not generally parasitic 

Animals 

Animals 

Animals 

Animals 

Animals 



PART INFESTED 



Wounds 

Wounds 

Skin 

Skin 

Wounds 



[us atratus 
us lineola 



Animals 
Animals 



Skin 
Skin 



la morsitans 



Animals 



Skin 



um pecuarum 



Animals 



Skin 



hagus ovinus 
•osca equina 



Sheep 
Horse 



Skin 

Skin around perinaeum 



philus equi 

philus hemorrhoidalis 

erma Ilneata 

H ovis 



Horse 
Horse 
Ox 

Horse 



M. M. of stomach 
M. M. of stomach and intestine 
Dorsal cutis and subcutis 
Sinuses of head 



lequinus 

pipiens 
bles punctipennis 

la fasciata 

ppinus macrocephalus 
>pinus eurystermnus 
jpinus vituli 
'jplnus piliferus 
}pinus irritans 
>pinus stenopsls 



Sheep 
Animals 
Animals 
Animals 

Horse 

Ox 

Ox 

Dog 

Pig 

Goat 



Skin 
Skin 
Skin 
Skin 

Skin 
Skin 
Skin 
Skin 
Skin 
Skin 



lectes pilosus 
lectes scalaris 
lectes spaerocephalus 
lestes latus 



Horse 
Ox 

Sheep 
Dog 



Skin 
Skin 
Skin 
Skin 



•I 

rritans 

erraticeps 

ivium 



Man 

Fowls 



Skin 
Skin 
Skin 



lus annujatus 
us Australis 
imma Americanum 
lentor electus 
doros Megnini 
riclnus 
tniniatus 



Ox Skin 

Ox Skin 

Ox Skin 

Sporting dogs Skin 
Horse, ox, sheep and dog Skin 

Sporting dogs Skin 

Fowls Skin 



lyssus gallinae 



Fowls 



Skin 



I Hum holosericeum 

' Irritans 

( 

5S scabei-var, equi. 

28 scabei var. ovis 

Bs scabei var. suls. 

9s scabei var. canis. 

ps mutans 

es communis var. equi. 

3 communis var. bovis. 

3S communis var. ovis. 

;ee scabei var. equi. 

es scabei varfl bovis. 

es scabei var. ovis. 
i es auricularum var. cani. 
i es aureicularls var. fells 



(x follicurlorum var. equi. 
i folliculorum var. bovis. 
X folliculorum var. cani. 



Animals 


Skin 


.Man and animals 


Skin 


Horse 


Skin 


Sheep 


Skin 


Pig 


Skin 


Dog 


Skin 


Fowls 


Skin 


Horse 


Skin 


Ox 


Skin 


Sheep 


Skin 


Horse 


Skin 


Ox 


Skin 


Sheep 


Skin 


Dog 


Skin 


Cat 


Skin 


Horse 


Skin 


Ox 


Skin 


Dog 


Skin 



ula taenloidea 



Dos 



Nasal cavities 



GENERAL CONSIDERATION OF DISEASE. 



71 




Fig- 44. — Melophagus Ovinus, after Niles. 

a. Dorsal view of adult, d. Terminal segment of leg. 

b. Ventral view of adult. e. Shell of pupa. 

c. Mouth parts enlarged. f. Pupa. 



horse louse (Trichodectes Pilosus) and feathers, e. g., the 
chicken louse (Menopon Pallidum) others abstract blood, e. g., 
the hog louse (Hematopinus Suis), Itch mite (Sarcoptes scabei 
variety canis), and still others may consume tissue cells other 
than blood cells as epithelium. Reproduction of arthropoda is 
about the same as it is in helminthes. 

Disease resulting from infestation of arthropoda is due 
primarily to irritation induced mechanically or by chemic pro- 
ducts of the parasites, secondarily to loss of blood. 




VETERINARY PATHOLOGY 



S 




Fig-. 45 — Part I. 
Gastrcphiliis Equi, after Niles. 
Adult female. 
Adult female. 
Young- larvae. 
Full gro-wn larvae. 
Eggs cemented to hair. 
Eg-g shell showing- lifting of 

operculum. 
Adult male. 

Terminal segments of male. 
Terminal segments of female. 









Fig. 45. — Part II. Oestrus Ovis. 

Adult female. c. Dorsal view of larva. 

Adult male, after Rily. d. Ventral view of larva, after Rily and Niles. 



GENERAL CONSIDERATION OF DISEASE. 



71 




Fig 47. — Culex Pungens, after Howard. 
a. Female. b. Male. c. Larva. 



74 



VETERINARY PATIICLOGY. 






Fig. 48. — Asearis Mystax, after -Niles. 



a. Adult male. 

b. Adult female. 



a. Cephalic extremity, 
d. Caudal. 



Extension of Disease. — By extension of disease is meant the 
invasion and affection of adjacent structures and even remote 
tissues of the body. Some diseases are necessarily local, i. e., 
the cause is not capable of being transferred to adjacent or re- 
mote structures, e. g., ocular filariosis. Other diseases are in 
their earlier stages local, but later the cause may be transferred 
to some other part and produce secondary diseased foci or 




Fig. 49. — Distoma 
Hepaticum. 

a. Intestines. 

b. Oral sucker. 

c. Ventral sucker. 

d. Uterus. 



metastases, e. g., tuberculosis. The extension of disease may 
be produced as follows : 

First, by the cause of thej disease passing along the natural 
channels and establishing secondary diseased foci, thus. Bray 
reports that calves become affected with necrotic gastritis and 



GENERAL CONSIDERATION OF DISEASE. 



75 



enteritis when allowed to swallow the necrotic tissue during- an 
attack of necrotic stomatitis. 

Second, by the spread of the cause into adjacent tissues, e. g: 
Extension in like tissue, as in muscular tissue, is continuity as 
psorospermosis, while extension from one tissue to another of 
a different type, as from muscular to connective tissues, is con- 
tiguity as in actinomycosis. 

Third, by the lymph and lymphatic nodes, e. g. tuberculosis. 



^^Pi^ 








Fig. 50. — Echinorynchiis Gigas, after Niles. 

a. Cephalic extremity showing hooks. 

b. Worm xvith Dortir>n nf rmifnns mpmhranf r>f intestirip. attaohed. 



Fourth, by the blood stream in which case the mestastases 
will be in the lungs, liver or kidney, — e. g. anthrax. 

Fifth,by passing along the nerve fibers as in rabies. 

Termination of Disease. — Termination is the ending or out- 
come of the condition or existing disease. Disease terminates 
as follows : — 

Recovery. — Disease terminates in recovery when the body 
tissues are effectually repaired and all structures have assimied 
their normal function. Diseases resulting from irritating or 
non-nutritious foods are corrected by expulsion or neutraliza- 
tion of the causative agent either by vomition, purgation or 
chemical union and by repair of the injured tissues, after which 
normal functioning continues. Tissue afflicted with mechanical 



76 



VETERINARY PATHOLOGY. 



injuries as wounds, recover wlien the destroyed portions have 
been replaced and the normal function has been resumed. Dis- 
locations terminate in recovery when the dislocations have 
been reduced and the parts assume their normal function. A 
horse recovers from pneumonia when the inflammatory exudate 
has been removed from the alveolar spaces and all injured 





Fig. 51. — Trichina Spiralis, after Colin. 




Fig. 52. — Tricliodectes Latus, after Niles. 
a. Dorsal view. b. Egg cemented to hair. c. Ventral view. 



GENERAL CONSIDERATION OF DISEASE. 77 

tissues have been repaired and the normal functioning has been 
re-established. In general, recovery is the result of the activi- 
ties of the protective and reparative processes of the various 
tissues of the animal body. 

Partial recovery. — If the normal funtioning is not assumed 
after a disease has run its course, recoverv is said to be incom- 
plete or partial. Partial recovery is observed in old animals or 
in those that have been depleted because of complications or 
previous disease. Some diseases are essentially destructive and 
their influence in the tissue results in incomplete repair, as in 
tuberculosis, glanders, dourine, bovine contagious pleuro-pneu- 
monia, etc. Injuries and acute inflammation of the parieties of 
hollow organs frequently terminate in the formation of cicatrical 
tissue thus contracting the lumen of these organs. This is com- 
mon in injuries of the oesophagus, intestine, trachea, and ure- 
thra. Adhesions succeeding pericarditis, pleuritis, and periton- 
itis are examples of partial recovery. 

Deatli. — Disease may terminate in the cessation of all func- 
tions, i. e. death. The more important specific modes of death 
are as follows : 

1. Syncope, or heart failure, a result of paralysis of cardiac 
nerves or muscles, rupture of heart walls or complete obstruc- 
tion to emerging vessels of the heart. Nerve paralysis may be 
the result of poisonous products derived from infectious agen- 
cies, or chemic poisons derived from katabolism, or hemorrhagic 
extravasates. 

2. Apnoea, or respiratory failure. This may be the result of 
paralysis of respiratory nerves or muscles, spasms of respiratory 
muscles, rupture of diaphragm, or occlusion of the respiratory 
tubes. 

3. Apoplexy, or hemorrhage into the brain tissue. This is 
probably the specific cause of death in apoplectiform anthrax. 

4. Hemorrhage, especially rapid loss of large quantities of 
blood. Any of the above may act independently in producing 
death, but are probably more frequently complicated one with 
another. 



CHAPTER III. 
IMMUNITY. 

DEFINIIION. 

IMPORTANCE. 

VARIETIES. 

Inherited, {Natural). 
Definition. 
Examples. 
Cause. 

Cell Action, {Metchnikoff & Sternberg). 
Chemic Substance, {Ehrlich & Buchner). 
ACQUIRED, (Artificial). 
Definition. 
Examples. 
Varieties. 
Active. 

Definition. 

Varieties, {Toxic), {Bacterial). 
Etiology. 
Recovery from attack of disease. 
Inoculation with virus. 
Inoculation with vaccine. 
Inoculation with bacterin. 
Inoculation with toxin. 

Inoculation simultaneously with virus and antibody. 
Passive. 

Definition. 
Etiology. 

Inoculation with antibody. 
THEORIES. 

E^fliaustion. 
Retention. 
Phagocytosis. 
Humoral. 
Ehrlich's Lateral Chain Theory. 

Immunity literally means proof against disease, i. e., it is 
the name of the condition that enables an animal to resist the 
action of pathogenic micro-organisms, or to be unaffected by 
their products. Immunity is only a relative term, the condition 
is not absolute and permanent neither is it constant and con- 
tinuous. Whenever an animal is unable to adjust itself to its 
environments it becomes susceptible to the effects of the causa- 
tive agents of diseases, i. e., its immunity, at least acquired 
immunity, is suspended. 

The term immunity is ordinarily used in reference to infec- 
tive diseases, i. e. those diseases resulting from the invasion of 
microparasites ; although it may be used in designating the 
resistance to the action of zootoxin, such as snake venom, and 
possibly also of the poisonous substances ejected by centipedes 

78 



IMMUNITY. 



79 



and scorpions, as well as the phytotoxins, such as ricin, abrin, 
crotin, and robin. 

Immunity, more than any other problem, directly concerns 
the medical profession and indirectly the international commer- 




Fig. 53. — Hematopinus phalanges ovis, after Niles. 
a. Adult. b. Egg cemented to hair. 

cial welfare. It was a laboratory fad of the pathologists until 
they demonstrated to the practitioners that it was feasible to 
produce immunity in man and animals. Veterinarians have now 




Fig. 54. — Pulex Serratioeps, after. Tu'.?ii:or- 



80 



VETERl N AR^' PATHOLOGY. 



almost universally accepted the proposition and have at their 
command the means by which they can immunize animals 
against the ravages of some of the fatal infective diseases to 
which they are susceptible. The increased confidence of the 
people is in turn enabling scientists to investigate new phases 
of the subject. Although immunization has been known and 
made use of more or less for centuries as vaccination against 





Margraranus Annulatus, female. 



Fig. 56. — Margarapus Annulatus, male. 




Fig. 57. — Margarapus Annulatus, 

female layin,? efn^s. 



Fii 




Margarapus Annulatus, Larva. 



smallpox by the Chinese before the Christian era, yet the essen- 
tial physiologic, chemic or pathologic basis for immunity is 
still unknown. 

Immunity may be natural (inherited) or artificial (acquired). 

Natural immunity is an inherited property possessed by or- 
ganisms (animals). The horse has a natural immunitv to hog 
cholera, the ox to glanders and the hog to tick fever. The 
concise and exact cause of natural immunity is unknown. It 
is probably the result of cellular activity in the immune animal, 
an activity the nature of which is not understood. Some inves- 
tigators, Metchnikofif in particular, attribute natural immunity 
to phagocytosis (cellular hypothesis), others maintain that Insus- 



IMMUNITY. 



81 



ceptibility to disease is a result of the antagonistic action of the 
body fluids (humoral hypothesis). Ehrlich's lateral chain the- 
ory assumes that the cells of immune animals are not capable 
of combining with the toxins of bacteria, i. e.. they have no 
receptor molecules and hence those animals are not receptive, 
they are immune. Whether we accept the cellular hypothesis, 
the humoral hypothesis, or Ehrlich's lateral chain theory, the 
fact remains that natural immunity is a characteristic or prop- 
erty of parental origin that is transmitted to the offspring and 
is present at the time of birth. 

Natural immunity may be the result of an acquired toler- 
ance due to natural selection and heredity. There is a marked 
variation in susceptibility and resistance in individuals of a given 
species. A continuous or repeated exposure of susceptible ani- 
mals to a given pathogenic microparasite will result either in 




Fig. 5 9. — Ixodes ricinus, female, after (B. A. I.) 



destruction of those animals or the production of an immunity, 
i. e,, those individuals least resistant will survive and their 
resistance will become more and more fixed and will finally be 
transmitted to the oiifsprmg and hence be a natural immunity. 
Thus all native Cubans are practically immune to yellow fever 
because at the time yellow fever was first introduced into Cuba 
ihe least resistant individuals died of the malady, the most 
resistant individuals survived and lived in the presence of the 
diseases almost continually after yellow fever was introduced 
into Cuba (It was not eliminated until after the Spanish-Amer- 
ican war). Consequently the Cubans for several generations 
developed in the midst of yellow fever and only the resistant 
individuals survived. This resistance finally became so firm 



82 



VETERINARY PATHOLOGY. 



that it was transmitted to their offspring and was then a nat- 
ural immunity. 

The resistance possessed by dogs to most diseases is ex- 
plained in a similar way to the Cubans' resistance to yellow 
fever. Thus the dog has descended from the jackal and the 
wolf, two types of animals that have lived largely upon the 
carcasses of animals dead of various diseases. As the animals 
fed on carcasses they fought, thus inoculating each other, so in 
the beginning the least resistant individuals died, the more resis- 




Fig. 60. — The scab mite of sheep, Psoroptes Communis Ovis, mag-nified 150 diameters. 



tant animals survived. Thus the constant fighting and inocu- 
lating has established in them a firm resistance that is trans- 
mitted to their progeny as a natural immunity. This immunity 
has become so fixed that it does not vary even in the domestic 
dog. The above is a plausible explanation of race or species 
immunity. The exact origin of individual immunity is considered 
by some to be an acquired tolerance, i. e., an acquired immunity, 
and by others, as simply an individual resistance not developed 
by having the disease to which the given individual is immune. 
Acquired immunity is an artficially produced condition b}^ 
virtue of which the animal is capable of resisting disease, and 



IMMUNITY 



83 



is produced in an animal either in utero or after birth, and may- 
be active, or passive, bacterial or toxic. 

Active acquired immunity is, no doubt, the result of cellu- 
lar action and may be produced as follows : — 

1. By an animal becoming- infected and recovering from an 
attack of the disease, e. g. blackleg. 

2. By inoculation of a susceptible animal with a small 
quantity of the virulent causative microparasites, thus produc- 
ing the disease in a mild form. This is practiced in immunizing 
cattle against tick fever. 




Fig. 61. — Demodex Folliculorum, 

vailety Canis. 
Field showing various stages of 
development. 

a. Ova. 

b. Pupa. 

c. Adult. 

d. A piece of Scab. 



Fig. 61a. — Demodex Folliculorum, 

variety Canis. 
Adult Male, magnified 400 times 
showing wide head, with ros- 
trum, short legs (3 articles each) 
2 claws and elongated body. 



3. By inoculating a susceptible animal with an attenuated 
virus, (vaccine.) Horses, mules, cattle, and sheep are immun- 
ized to anthrax by a vaccine. 

4. By repeated inoculations of a susceptible animal with 
small quantities of a toxin of a specific pathogenic microparasite. 
tetanus toxin or other active poison as snake venom. This 
method is used only in the production of antitoxins or in immun- 
izing animals against zootoxins and phytotoxins. 



84 VETERINARY PATHOLOGY. 

5. By simultaneous inoculation with a virus and an antitoxin 
(antibodies, bactericidal substances, etc.) In the Philippine 
Islands this method is employed in immunizing cattle against 
rinderpest, and it is also being successfully used in the immun- 
ization of hogs, against cholera. 

Toxic immu.nity is the resistance to poisonous substances as 
toxins of bacterial origin, zootoxins and phytotoxins. It is 
common to hear sheep herders speak of dogs that are immune 
to the venom of rattlesnakes. The dogs are bitten frequently 
while doing duty on the range and although the reaction from 
the first inoculation is intense and may even kill, each succeed- 
ing inoculation produces less reaction until finally the dogs may 
be bitten or the venom inoculated with impunity. Immunity to 
intoxication diseases such as tetanus are of this type. The ab- 
sence of action of various therapeutic agents that have been 
given repeatedly may be explained on the principles similar 1o 
those involved in the production of immunity in dogs to snake 
venom. Toxic immunity is the result of the presence in the 
body fluids of an antibody (Antitoxin.) 

Bacterial immunity is the resistance an infected animal 
manifests to the bacterial invader. It is the result of bacteri- 
olytic substances in the body fluids. Pfeififer demonstrated that 
bacteria are destroyed when introduced into an immune animal. 
He introduced the spirilla of Asiatic cholera into the peritoneal 
cavity of guinea pigs and noted that the bacteria were soon 
rendered immobile, became swollen and granular and were fin- 
ally disintegrated. This phenomena has been designated Pfeif- 
fer's reaction. 

Passive acquired immunity consists essentially of the presence 
in the tissues or body fluids of substances inimical to micro- 
parasitic activity, or substances capable of union with micro- 
parasitic products, (toxins) thus rendering them inert. This 
type of immunity is of short duration. It is usually produced 
by the inoculation of susceptible animals with antitoxin. Injured 
'. animals inoculated with tetanus antitoxin at the time of injury 
are thus immunized to tetanus for a brief period. 

Acquired immunity, like natural immunity, is variable and 
inconstant. The production of active acquired immunity entails 
more risk than the production of passive acquired immunity. 
The causative agents or their toxic products are used in obtain- 
ing an active immunity and thus disease may be produced and 
the animal life sacrificed while the anti-toxin is used in the 
production of a passive immunity, without danger of the pro- 
duction of disease although transient disturbances may result 



IMML'NITV. 



85 



from hemolysins, contained in the blood in which there is anti- 
toxin. 

Theories of acquired immunity. — Many theories have been 




itf: .',*.■.••:- •, ' • . •••:•■•• I.VH'X 

i:} -i ••■.".: • ... • • • . .-. ■•;•'>) 
i<*i'.". ' •■ , • . ' ■ . • . '••■•.■••', ".V 

W-vv,i<'.' « . • ■ • « . ^i' •' • \ •••^ •• :y 

►•^^i". •- '.• . ' ♦ .. » •'••s.-'-'y7 

\;:^A^•,^ *;••.■•'■ •■••.' • ■*':■• ."'-'vvTdrij 
Xj'S- •:';'.> • *'•■ -•• ••••••• Y'^.^W 





Fig. 62. — Bacterial Immunity. 

Legend — c Amboceptor. 

a. Cell body. o. Compliment 

b. Cell receptor. 



advanced in explanation of acquired immunity. The chief of 
whicli are as follows : — 



86 



VETERINARY PATHOLOGY. 



1. The Exhaustion Theory. — This theory was championed by 
Pasteur, who proposed it about 1880. It is based upon the 
supposition that there are certain substances in the animal body 
that are food for micro-parasites and that these substances are 
not regenerated. Hence when they have been consumed the 
micro-parasites cease to develop and the animal becomes im- 
mune. This theory is not tenable because immunity can be 
produced bv bacterial products and by dead bacteria neither of 




YU 



63. — Hematoba Serrata, after Riley and Howard. 

a. Egg-. c. Pupa. 

b. Larva. d. Adult fly. 



which consume substances from the tissues of an animal immun- 
ized. 

2. The Retention Theory. — In the study of bacteriology it 
has been found that bacteria, like most other organisms, can 
not develop in the presence of a large quantity of their own 
excrements. This theory presupposes that bacterial products 
remain in a body after it has been infected and that these 
products prevent the future development of like bacteria. This 
theory does not explain the production of an immunity with 
toxines and is not supported by any scientists at the present 
time. The theory was proposed by Chauveau. 

3. The Phagocytosis Theory. — ^This theory was proposed 
independently by Sternberg and Metchnikofif about 1881. The 
theory was the outgrowth of the experimental study of the 
action of leucocytes upon bacteria and yeast, in wdiich it w^as 



IMMUNITY. ^ 

found that certain leucocytes are active in the destruction of 
various bacteria, yeast and tissue debris. These investigators 
designated those leucocytes active in the destruction of bacteria, 
phagocytes. Phagocytosis is a state or condition characterized 
by the development of phagocytes and the display of their 
special function. The supporters of this theory hold that the 
cells, which are active in the production of leucocytes transmit 
the property of phagocytosis to their progeny and thus immun- 
ity is perpetuated after it has been acquired. That phagocytes do 
incorporate bacteria and other foreign substances is not denied 
but it has not been demonstrated whether phaogocytosis is the 
cause- or the result of immunity. 

This theory does not explain immunity from such diseases as 
tick fever. The microzoon of tick fever inhabits and usually 
destroys the red corpuscles. The leucocytes are probably not 
affected by them. In fact, the presence of the Piroplasma bigem- 
inum in leucocytes has not been noted. More recently Wright 
and Douglas have demonstrated that certain substances in the 
blood serum are necessary to prepare bacteria for phagocytic 
action. These substances have been designated opsonins." 
Opsonins are chemic substances in blood serum that render 
bacteria subject to the action of phagocytes. Opsonins resem- 
ble the amboceptors of Ehrlich in action, but they are not iden- 
tical with them. The action of opsonins is evidenced in pneu- 
monia, pyogenic infections, tuberculosis and probably in other 
diseased conditions. The opsonic index indicates the relative 
power of resistance due to phagocytic action in an animal body. 

4. Humoral theory. — After the phagocytic theory had ben 
found insufficient, immunity was explained from a chemic viev.^ 
point. The supporters of this theory, among whom Buchner 
was active, demonstrated the bactericidal action of blood serum 
and lymph obtained from immune animals. Their demonstra- 
tions established the fact that immunity is due to a chemic 
substance, possibly an enzyme. But the origin and specific ac- 
tion of the chemicals in the production of immunity was not 
determined. The bacteriolytic substance of the body fluid called 
complement, was found to be destroyed by a temperature of 
55°C. 

5. Ehrlich's Lateral Chain Theory. — Ehrlich maintains that 
every living cell contains an active central body and an indefin- 
ite number of marginal chemic groups or lateral chains desig- 
nated receptors. These receptors combine with and extend the 
nutriment to the central portion of the cell. The receptors are 



88 



VETERINARY PATHOLOGY. 




Fig. 64. — Uncinaria Canina. Cephalic extremity of female, magnified 

350 diameters, 
a. Hooklets. b. Mouth cavity. c. Oesophagus. 





Vx1 



Fig. 64a. Fig. 64b. 

Fig. 64a. Section of body of female, magnified 100 diameters, showing the 
the ova to have formed in worm not to exceed five weeks old. 
a. Ovum. b. Intestine. 

Fig. 64b. Caudal extremity of the female, magnified 100 diameters. 



also capable of combination with other substances as bacterial 
toxins. 

Toxic immunity is explained by Ehrlich as follows : Toxins 
are composed of two essential chemic groups which are desig- 



IMMUNITY. 



89 



nated haptophores and toxophores. The haptophore of the 
toxin has an affinity for the cell receptors. The union of the 
toxin haptophore and the cell receptor forms a medium through 
which the toxin toxophore passes to the central part of the 
cell where it exerts its action. 




Fig. 65. — Toxic Immunity. A cell showing active central body and marginal 
chemic receptors, and toxin molecules surrounding It. 
Legend — 

a. Cell body. 

b. Cell receptors. 

c. Free cell receptors. 

d. Haptophore of toxin molecule. 

e. Toxophore of toxin molecule. 

f. Toxin molecule. 

g. Toxin molecule combining with free cell-receptor. 

h. Toxin molecule floating free and about to combine with a free 
cell-receptor. 



The toxin haptophores are not injurious except as they enable 
the destructive toxin toxophore to reach the central cell mass. 
Toxin toxophores in the absence of toxin haptophores are inac- 



90 VETERINARY PATHOLOGY. 

live. The result of the union with, or action of, the toxin toxo- 
phore upon a cell may produce immediate destruction of the 
cell or it may stimulate the cell to produce more receptors. The 
presence of toxin in the body fluids stimulates the body cells 
to produce receptors in excess. The increased receptors may 
remain in connection with the central body or they may become 
detached and float in the body fluids. Free receptors in blood 
serum is the essential active principle of antitoxin. Toxic im- 
munity may be better understood by giving an example. 

Example. — Tetanus is an intoxication disease due to the pro- 
duction of toxins by localized bacterial activity of the tetanus 
bacillus. Immunity to tetanus is dependent upon the neutraliza- 
tion of the tetanus toxin. The tetanus toxin is composed of hap- 
tophores and toxophores. The body cells possess receptors caba- 
ble of union with the tetanus toxin haptophores. The union of 
cell receptors and tetanus toxin haptophores enables the tetanus 
toxin toxophore to act upon the central mass of the body cell, 
thus stimulating them to form more receptors. The excess recep- 
tors become detached and float free in the body fluids and com- 
bine with the tetanus toxin haptophore, thus preventing the lat- 
ter from combining with the attached cell receptors. The te- 
tanus toxophores are not capable of combining with the central 
mass of the body cells except through the medium of tetanus 
toxin haptophores and if the tetanus toxin haptaphores are 
locked up with the detached cell receptors, the tetanus toxo- 
phores remain inactive and the animal is not inconvenienced by 
their presence and is immune. 

Toxic immunity is therefore dependent upon first, suflicient 
free receptors to lock up the haptophores thus inhibiting the 
action of the toxophore or second, upon the absence of hapto- 
phores. 

Bacterial immunity. — From the phenomena observed in Pfeif- 
fer's reaction Ehrlich has proposed an hypothesis in explanation 
of bacterial immunity. As previously stated, normal blood serum 
contains bacteriolytic substances (see humoral theory). Comple- 
ments are destroyed by a temperature of 55°C. The blood serum 
of immune animals possess another substance, in addition to 
complement, not destroyed, by heating to 55°C. These are called 
amboceptors. According to Ehrlich, amboceptors, like toxins, 
are composed of two different combining groups, also designated 
haptophores and toxophores. The complemental substance of 
normal serum is not capable of action upon bacteria. The ambo- 
ceptor haptophore has an affinity for" the compi^ment of normal 
serum. The amboceptor toxophore has an aflinit}^ only for bac- 



IMMUNITY. 91 

teria, but is not injurious to them. The amboceptor toxophore 
combined with or acting upon bacteria produces a condition 
favorable for the action of the combined amboceptor haptophore 
and complement, i. e,, this enables the complement to cause dis- 
integration of bacteria. The amboceptor thus renders condi- 
tions favorable, i. e., makes it possible for the bacteriolytic sub- 
stance, the complement, to exert destructive action upon bacteria^ 
the amboceptor acting as middle man. 



CHAPTER IV. 

MALFORMATIONS. 

DEFINITION. 
ETIOLOGY. 

Intrinsic {heredity.) 
Extrinsic. 

Pressure. 

Amniotic Adhesion. 
Excessive Motion. 
LIclnutrition. 
CL.ASSES. 
Single. 

Result of Arrested Developement. 
Result of Excessive Developement. 
Result of Transposed Visceral Orgnas. 
Result of Persistent Foetal Structures. 
Result of Mixed Sexual Organs. 
Double or Multiple. 
Symmetrical Duplicities. 
Complete (twins). 
Incomplete (double monster). 
Asymmetrical Duplicities. 
Multiple. 

During the embryonic stage of intra-uterine life the special- 
ized tissues and organs are formed. The foetal period is the time 
during which the structures formed in the embryonic stage grow 
and develop. At birth the young of a given species are of <a 
definite shape, contour and type ; the form or type which is most 
common is accepted as normal ; and deviations from the normal 
are designated malformations, anomalies or developmental 
errors. Many new strains and breeds of stock have been the 
result of developmental errors becoming a fixed peculiarity. 
Thus the polled cattle, the Boston bull-dog, the Mexican (hair- 
less) dog, and the five toed chicken had their origin. 

Etiology. — Malformations may be brought about by pre- 
existing influences in the maternal cells, (internal or intrinsic 
causes), or from external influences (external or extrinsic 
causes). 

Internal or Intrinsic Causes. — Internal causes are inherited 
peculiarities, i e., heredity and atavismal influences. These are 
probably not the usual causes of malformation in domestic animals 
for malformed individuals are rarely used for breeding purposes. 

External or Extrinsic Causes of malformations are pressure, 
amniotic adhesions, excessive motion, insufficient or abnormal nutri- 

92 



MALFORMATIONS. 93 

tion, infectious diseases, etc. External causes exert their in- 
fluence during the embryonic or formative period and they 
must act in a mild degree or death of the embryo and abor- 
tion follows. 

Typical malformations are approximately of the same form 
and are usually produced by similar causes. Atypical mal- 
formations are variable in form and may be produced by a 
variety of causes. 

A complete description of all malformations is beyond the 
scope of general pathology. A general classification with a 
description and origin of the most striking malformations is 
all that will be attempted in this chapter. 

Malformations may be divided into two classes ; 1st, Single 
malformations, and 2nd, Double or multiple malformations. 

Single malformations are those aitecting a single individual. 
Single malformations mav be grouped into five classes as fol- 
lows : ^^lalformations resulting from; (a) arrested growth or 
development ; (b) excessive growth or development ; (c) trans- 
position of visceral organs; (d) persistent foetal structures; (e) 
mixture of sexual organs. 

ARRESTED DEVELOPMENT. — Alal formations caused by arrested 
development may involve an entire individual or any phrt of 
an individual. Arrested development of the entire individual 
results in the formation of an irregular, fleshy mass, called a 
mole, in place of the normal foetus. IMoles may be carried in 
the uterus for the entire period of gestation. In some instances 
a mole and a normal foetus may be delivered at the same time. 
Moles have been observed in mares, more rarely in cows. 

Malformations resulting from arrested development of a part 
may be manifested by the entire absence of the part (aplasia), 
by underdevelopment of the part, (hypoplasia), or by a lack 
of union or fusion of tissue (schistosis and atresia). The fol- 
lowing malformations are the result of local aplasia. 

Acephalus. A name applied to a headless monstrosity. 
Acephalus is probably the result of amniotic adhesions. 

Atrichia. A defect in which there is no hair. This results 
from some disturbance of cutaneous development. 

Amyclus. A malformation in which the spinal cord is absent. 
Defects of the primitive streak or failure of production of the 
neural canal interferes wdth or prohibits the formation of the 
spinal cord and is the cause of amyelus. 

Acardia. A heartless monstrosity. 

Agastria. A malformation in which the affected i-ndividual 



94 VETERINARY PATHOLOGY. 

has no stomach. This may be due to lack of sacculation of the 
embryonic gut. 

Acaudia. A malformed individual in which the defect con- 
sists in the absence of the tail. An acaudia fox terrier bitch 
was recently observed, her mother whelped one or two tailless 
puppies at each whelping. This bitch recently whelped an 
acaudiac puppy. 

Aprosopus. An individual having no face. 

Agnathus. A term used to designate an individual in which 
the inferior maxilla is absent. This is common in lambs. 

Amelus. The name of a limbless or legless individual. Amelus 
is the result of arrested development of leg buds and is usually 
caused by unequal intrauterine pressure or amniotic adhesions. 

Monopygusamelus. A monstrosity in wihich one posterioi 
leg is wanting. This is due to arrested development of leg buds, 
probably due to amniotic adhesions. 

Dipygusameliis. The name of a malformed animal in which 
both posterior legs are absent. Result of arrested development 
of leg buds. 

Monothoracisamelus and dithoracisamelus are monstrosities 
in which one and both front legs are absent respectively. 

Apus. A name applied to a malformation in which the feet 
are absent. This may be the result of intrauterine amputation 
or amniotic adhesions. 

Monopygnsapus is aa individual in which one hind foot is 
wanting and a dipygusapus, an individual in which both hind 
feet are absent. 

Monothoracisapus, and dithoracisapus, are names implying 
the absence of one or both front feet. 

The following malformations are the result of under develop- 
ment or undergrowth. (Hypoplasia). 

Microcephahis, a term used to designate an individual hav- 
ing a diminished sized head, also used to designate the small 
head itself. This is probably the result of diminished nutrition 
to the head and anterior part of the body during embryonic and 
foetal development. 

Micro-cardia. A name applied to an individual having a 
small heart. This may be due to excessive pressure. 

Microophthalmia. A term used to indicate a malformation in 
which the eye or eyes are smaller in size than the normal. This is 
probably the result of insufficient nutrition. 

Micrognathy. The name of an individual having a diminu- 
tive inferior maxilla. These are caused by undue pressure or 
insufficient nutrition. » 



M ALEORAIATIO N S . 



95 



Micromeliis. A malformation so named because of the 
diminished size of all legs. This is caused either by diminished 
nutrition or undue pressure. 

The following are illustrations of arrested development mani- 
fested by absence of imperfect tissue union, thus producing 
fissures (schistoses), or resulting in fusion of parts that are 
normally separate (synactoses). Fissures of the body cavities 
are due to increased accumulation of fluids in internal organs, 
increased size of internal organs, prolapse of viscera before 
body walls have united, the presence of amniotic folds betw^een 
cleft edges or lack of sufficient tissues to close the margins. 

Cranioschisis. The name of a condition produced by fail- 
Mire of development and union of the cranial bones and resulting 
in a cleft. The meninges and in some instances the brain 
tissue may be exposed or there may be protusion of the menin- 
ges and also of the nerve tissue, thus producing meningocele 
or meningo-encephalocele. 




Fig-. 66. — Cranioschisis — Calf. 



Cmniorrhachischisis. A malformed individual so called be- 
cause of a fissure of the spine and cranium accompanied by 
exposure or protusion of the spinal cord and brain. 

Rhachischisis. A condition i.n which there is a cleft of the 
spinal column. This malformation is usually the result of some 
defect in the margins of the neural groove. If the fissure ex- 
tends the entire length of the spinal column the resulting con- 
dition is called holoschisis. If the fissure does not extend the 



96 



VETERINARY PATHOLOGY. 



entire length of the spinal column, the condition is termed 
meroschisis (Gr. Meros==part, and schisis=!splitting.) The 
spinal meninges may protrude through the spinal column fissure 
producing spina-bifida. A hernia of the spinal meninx that con- 
tains cerebrospinal fluid is termed spinal meningocele, and if the 
cord and meninges protrude, it is called a myelomeningocele. 




Fig. 67. — Cheiloschisis. 



Cheiloschisis. is the condition resulting from arrested de- 
velopment of the soft tissues covering the maxilla. This is the 
condition popularly termed hair lip. It is an inconvenience 
because it interferes with sucking the teat, the source of nutrient 
of the new born mammal. The defect may also involve the 
maxilla producing cheiliognathoschisis. 

Palatoschisis. A defect in which the palatine processes have 
imperfectly developed, thus leaving a fissure through which 



MALFORMATIONS. 



97 




Fig. 68. — Palatoschisis. 



(there is free communication between the nasal and buccal 

cavities. This condition is commonly spoken of as cleft palate. 

Thoracoschisis. A condition resulting from failure of union 

of the thoracic walls. The thoracic viscera, the lung, heart and 




Fig. 69. — Abdoniinoschisis. 



98 



VETERINARY PATHOLOGY. 



large vessels may protrude through the fissure thus producing 
ectopiacordis or ectopiacordispulmonaris. 

Ahdominoschisis, is the condition caused by failure of union of 
the abdominal parieties. The. condition is frequently accompanied 
by protusion of the abdominal viscera through the fissure. The 
abdominal fissure may involve only a portion of the cavity or 
it may be complete. Ectopia gastrium is the condition result- 
ing from protrusion of the stomach through an abdominal 
fissure ; ectopia vesicae, protrusion of bladder, etc. 




Fig. VO. — Synophthalmia or Cyclopia. 



S'ynoynophthalmia, or cyclopia (Gr. Kuklops= mythical single 
eye monster), is a condition resulting from the fusion of the 
optical vesicles. Arrested development of the anterior cerebral 
vesicles allows the optical vesicles to contact and in some in- 
stances there is one large double eye centrally located or there 
may be two eyes occuring in a centrally located orbit. Cyclo- 
pia is usually associated with defects of the nose. 

Synactosis, is a general term denoting a coindition caused by 
the fusion of parts or organs that are normally separate. 

Synmelus. A malformation caused by the fusion of two legs 
into one irregular member. 

Syndactylus. An individual having the digits fused or grown 
together. An illustration of syndactylism is the soliped hog. 
The soliped hog usually has two separate digits of three 
phalanges each and the ossa pedes are encased in a single hoof. 



feet. 



Synmehisdipiis. A malformation having fused legs and two 



MALFORMATIONS. 



99 



Synmelnsmonopiis . An kidividual having fused legs and only 
one foot. 

Synmelusapits. A monster having fused legs and no feet. 

Synorchism. A malformed animal in which the testicles are 
fused. 

Arrested development may be evidenced by the nonappear- 
ance of the lumen in any of the natural hollow organs, (atresia). 
The mouth is formed by an ingrowth of the ectoderm and the 
buccal cavity extends inw^ard until it meets the anterior elonga- 
tion of the embryonic gut. Later the partition separating the 
buccal cavity and the cavity of the embryonic gut is absorbed 




Fig. 71. — A condition of Solinedia in a hog. 



and thus the cavities become continuous. Failure of the exten- 
sion of the mouth cavit}^ and its fusion with the embryonic gut 
constitutes the condition. Atresia Oris. 

Atresia iridis. A defect in the eye due to the absence of an 
opening (pupil). 

Atresia ociili, a malformation in which there is no opening 
between the eyelids. 

Atresia amis is a condition in which there is an imperforate 
anus, that is, there has been failure of union and fusion of the 
anal ingrowth and the rectal outgrow^th. Atresia anus is of 
rather frequent occurrence and usually the defect is easily re- 
lieved. 

Atresia urethra. Imperforation of the uretnra. 



IGO 



VETERINARY PATHOLOGY. 



MALFORMATIONS RESULTING FROM EXCESSIVE DEVELOPMENT OR 

OVERGROW^TH. — .Excessivc development is usually evideri^ced as a 
multiplicity of digits or phalanges though there may be multiplicity 
of any structure. 

Polydactylism. — The name applied to a malformed individual 
in which there is an excessive number of digits. Individuals 
having supernumerary digits are frequently observed. The 
condition is probably more frequently observed in hogs than 
in other animals. Polydactyli.sm, however, occurs occasionally 
in the ox and horse. 




Fig. 72. — Polydactylism in a hoj 



Polymehisthoracicits. — This is a malformation in which the 
affected animal has one or more extra front legs. An interest- 
ing case was observed in a cow in which there was an irregular 
bone attached to the right scapula, and extending across the 
median line. This bone articulated with an irregular supernum- 
erary scapula and also with the spine of the left scapula. This 
irregular formed scapula articulated with another bone which 
was similar to a humerus on the distal end of which there was 
a rudimentary ulnar. The condition of supernumerary posterior 
legs is termed polymeluspygus. 

Dicandis. — An individual having two tails. This type of 
malformation is not very common. It is probably the result of 



MALFORxMATIONS. 



101 




Fig. 73. — Prognathism, common name "undershot. 



a division or cleavage of the caudal segments during embryonic 
formation. 

Multiplicity of internal organs is occasionally observed. Thus 
several cases of partially double spleens have been reported. An 
interestinor case of malformation was observed in a hog, the defect 



102 



VETERINARY PATHOLOGY. 



consisting of a double penis. This individual may have been 
called a dipenis. 

; Malformations from excessive growth may be applied to the 
entire animal when it is excessively large (giants). Malforma- 
tions resulting from overgrowth of a part are frequent ; thus 
one foot, one leg, the head or any other part may be overgrown. 
Darwin, (in Plants and Animals under Domestication), men- 
tions 'a cat that he observed which had incisor teeth one and 
one half inches in length. 




Fig. 74. — Hehistosis melus anticus or diiiielus anticus — Male. 
(Drawing made from a photograph.) 



TRANSPOSITION OF VISCERAL ORGANS, (situs visccrum iuvcrsus-. 
Very rarely animals are observed in which the visceral organs 
are re-arranged, i. e., tliose organs that normally occur on the 
left side of the body are found on the right side. A sheep in 
prime condition was observed which was normal in appearance 
except its head was turned slightlv to the left and the atlas was 
ankylosed to the occipital, thus giving it but little vertical 
motion. The right shoulder was anterior to the left. The vis- 
cera were entirely reversed ; the heart was hanging toward the 



MALFORMATIONS. 103 

right : the four compartments of the stomach were transposed, 
the rumen being- on the right side, and the spleen being in con- 
tact with the right side of the diaphragm ; the liver was on the 
left side and the right kidney was posterior to the left which 
was swinging free as the right usually does. 

Transposition of visceral organs probably results from an 
irregularity of the allantoic veins and their continuation. In 
normal development the right vein atrophies and the left vein 
becomes larger in early embryonic life and if for any reason 
the left vein atrophies and the right vein becomes longer then 
the visceral organs tend to develop in the reverse position. ^ 

PERSISTENT FOETAL STRUCTURES, — All the malformatious are 
grouped into this class that retain embryonic or foetal structures 
abnormal to extra-uterine forms of life. 

Cryptorchids — (Gr. Kruptein — to hide and orchis-testicle) are 
probably the most frequent malformations resulting from the 
persistence of a foetal structure. The testicles of domestic ani- 
mals are formed within the abdominal cavity during embryonic 
life and later migrate, except in fowls, birds, etc., to their per- 
manent position in the scrotum. Cryptorchids are animals in 
which the testicle was properly formed, but did not descend 
to the scrotum. Dr. DeWolf carefully inspected 4671 male 
hogs and found 28 single and 7 double cryptorchids. 

Cloacal Persistence. — During embryonic life the rectum and 
urogenital tract terminate in one common cavity known as the 
cloaca. The cloaca persists throughout life in the avidae, but 
not in mammalia. H. Brassy Edwards, M. R. C. V. S., reported 
a case in the veterinary Journal of an imperforate anus in a 
brindle bull bitch pup 10 days old. There was no trace of an anus 
and the prominence usuallv felt in the perineal region of imper- 
forate anus was also absent. On operation the rectum and 
uterus were found to be fused, thus producing a cloaca. Dr. P. 
Phillipson of H'olbrook, Nebr., reported a colt in which there 
w^as a cloacal formation. In this case the floating colon fused 
with the uterus and the vagina was a common opening of the 
digestive tract and the genito-urinary tract. 

Cervical ectopia cordis. — This is the name of a malformation 
in which the heart is located in the cervical region. The heart 
is normally formed in the cervical region and if the anterior 
thoracic Avail closes prematurely, the heart remains in that re- 
gion. 

MIXTURE OF SEXUAL ORGANS, HERMAPHRODITISM. — The SCXUal 

glands, ovaries and testicles, and the external genitals, of both 



104 



VETERINARY PATHOLOGY 



-?-7T 










sexes, are derived from four similar embryonic structures. The 
influence or factors determining sex are not known. During 
embryonic development the sexual determination is not distinct, 



MALFORMATIONS. 105 

the individual possessing more or less complete se-xual organs 
typical of both the male and the female. Animals in which 
there is a combination of sexual organs are termed hermaphro- 
dites. According to the development of sexual organs, herma- 
phrodites are designated as true and pseudo or false herma- 
phrodites. 

A true hermaphrodite possesses secreting sexual glands of 
both sexes, i. e., they have secreting ovarian and testicular tis- 
sues. The external genitals of the true hermaphrodite may be 
bisexual or unisexual. True hermaphrodites are rare, and fer- 
tility of such animals is doubtful. True hermaphroditism may 
be lateral, bilateral or unilateral. 

Lateral hennaphroditisni is the condition in which there is 
an ovary on one side and a testicle on the other. The follow- 
ing example illustrates this type. The animal was a two year 
old bovine and had an ovary suspended by the left broad liga- 
ment and a testicle suspended by the right broad ligament. 
The two glands had their normal appearance, typical of ovarian 
and testicular tissues. This type of hermaphroditism is rare. 

Bilateral hernmphroditism is typified by the presence on 
both sides of an ovary and a testicle, or a single organ on each 
side containing ovarian and testicular tissues. This type of her- 
maphroditism, also is rare. 

Unilateral hermaphroditism is characterized by the presence 
of a single organ, as an ovary or testicle on one side and an 
ovary and testicle on the other side or an organ containing ovar- 
ian and testicular tissue on one side. This type is not common. 

Pseudo or false hermaphrodites are individuals having one 
distinct type of sexual glandular tissue and in which the exter- 
nal genitals partake of the nature of both sexes. This type of 
malformation is more common in the male and is usually the 
result of persistence of IMiillers canal and the further develop- 
ment of the uterus and Fallopian tubes. In pseudohermaphro- 
ditism the testicles are usually retained in the abdominal cav- 
ity. There are usually Fallopian tubes, vagina and uterus, the 
completeness of which is variable. The appearance of the testi- 
cle is variable according to the development of the female 
external genitals. Pseudohermaphroditism is much less fre- 
quent in the female than in the male. 

A rather well marked case of a pseudohermaphroditic horse 
was obtained and carefully observed for some time after which 
it was destroyed and the type and relation of the sexual organs 
were determined by dissection. In this animal the head and 
neck while not decisive of either sex in general rather favored 



106 VETERINARY PATHOLOGY. 

the male in conformation. There was quite a well marked 
vulva and the much elongated clitoris projected about four 
inches postero-inferiorly and closely resembled a penis. The 
uterus was quite rudimentary and the reproductive glands were 
located near the normal location of the in=ternal inguinal ring 
and had very little resemblance to either testicle or ovary. 
Microscopic examination did not solve the difficulty for the 
glands were a conglomerate of small cysts. The mammary 
gland was fairly well developed. 

Double or Multiple Malformations. — Under this caption 
those malformations will be considered that involve two or more 
individuals developing simultaneously. Marchand's classifica- 
tion of duplicate monsters is adhered to in the following discus- 
sion. The entire subject of duplicate monsters may be subdi- 
vided into 1st, symmetrical duplicity, 2nd, asymmetrical dupli- 
city, and 3rd, multiplicity. 

SYMMETRICAL DUPLICITY. — The individuals, in symmetrical 
duplicity are, in the beginning, similar and symmetrical. Each 
of the symmetrical duplicates is derived from separate, similar, 
equal anlagen of a single fertilized ovum or bisection of a single 
anlagen. This class of malformations may be divided into two 
groups : — viz., complete and incomplete duplicities. 

Complete Duplicity. — Complete duplicates are in the begin- 
ning alike and complete and the individuals may remain sep- 
arate thus forming twins, (free duplicities,) or they may be^ 
united, thus forming double monsters. 

Twins, (free duplicates), develop in a single chorion though 
each individual usually has a separate amnion and allantois. 
Monochorionic duplicates may develop equally or unequally, 
depending upon the division of nourishment. The above dis- 
cussion primarily applies to uniparous animals. However, by 
varying the number it is equally applicable to multipares. 
Twins also result from sim.ultaneous fertilization of two ova. 

Double monsters are mono-chorionic duplicities in which the 
bodies are united. The two bodies may be equal or unequal in 
size, depending upon the distribution of nourishment. Double 
monsters are the result of partial fission of a fertilized ovum, 
partial fusion of two separate anlagen of a single ovum, or par- 
tial fusion of two fertilized ova. The attachment of the two 
bodies of the double monsters may be posterior, middle or anter- 
ior. 

Posterior union may be dorsal or ventral. In the former the 
union occurs at the pelvis, and the dorsal surfaces of the bodies 
are usually in apposition, such a monster is called a pygopagus. 



MALFORMATIONS. 107 

Pygopagi have two umbilical cords which fuse to torm a single 
cord ; coccyx and sacrum are single, rectum and anus usually 
single ; spinal cord double anteriorly, fused posteriority form- 
ing a single filum terminale ; urogenital system usually double. 
Ventral posterior union may be confined to the pelvic region, 
(ischiopagus). or it may extend anteriorly to and including the 
thoracic cavity, (thoracisischiopagus). The two bodies in ven- 
tral posterior union are so united that their venter surfaces are 
in apposition. Ischiopagi, usually have a single umbilicus and 
cord; pelvic organs may be single or multiple; there is usually 
no anus. If one of the bodies is small or rudimentary, it is desig- 
nated a parasite, (ischiopagusparasiticus). Thoracoischiopagi, 
may have single or double thoracic viscera ; the abdominal vis- 
cera are usually double. -»^+s^ 
Middle union in double monsters occurs on the venter sur- 
face from the umbilicus and extends anteriorly. There is usu- 
ally a single umbilicus ; the abdominal viscera is usually double ; 
thoracic viscera single or double, depending upon the area of 
union ; middle union may occur at the xiphoid cartilage, (xipho- 
pagus), involve the entire sternum, (sternopag-us), or the entire 
thoracic venter surface, (thoracopagus), xiphopagi mav survive, 
the "Siamese Twins,'' were of this type. Thoracopagi are fre- 
quently unequal in size, the smaller one being designated as a 
parasite. 

Anterior union may be dorsal or ventral or the union may be 
on the anterior surface of the head. Dorsal, anterior union 
rarely occurs, the attachment being on the frontal region. These 
malformations are designated Craniopagi. Ventral anterior 
union occurs occasionally. The union in this type is along the 
venter cervical region and extends onto the venter thoracic re- 
gion. The sternum and oesophagus are single; larynx, trachea 
and stomach may be single or double; intestine double; there 
may be two faces or the faces may be fused. Fused-face mon- 
sters resulting from union of the venter anterior cervical or 
cephalic regions are called syncephali. 

Incomplete Duplicity is the name applied to those malforma- 
tions in which the greater part of the body is single, duplica- 
tion occurring in only a part. The duplicity may involve any 
part. These malformations are not easily differentiated from 
malformations resulting from multiplicity of parts as polydacty- 
lism. 

ASYMMETRICAL DUPLICITY are thosc malformations result- 
ing from the development of two separate, dissimilar, unequal 
anlagen of a single ovum, the development of a fertilized polar 



108 



VETERINARY PATHOLOGY. 




Fig. 76.— Dicephalic Calf. 




Fig. 77. — Dicephalic Calf. 



MALFORMATIONS. luJ 

body or the development of an isolated group of segmentation 
cells. In asymmetrical duplicity one body is rudimentary or 
under-developed, (the parasite), and the other body develops 
normally or nearly so, (the autosite). The parasite always 
remains attached to the autosite or is included by it. Parasitic 
duplicity may occur in any region. Thus the parasite may pro- 
ject from the orbit, mouth, shoulder or it may be included in 
the thoracic or abdominal cavities. 

MULTIPLICITY is the name applied to designate the develop- 
ment of more than two separate individuals in a single chorion. 
Multiplicity is of rare occurrence. One single case has been 
authentically reported in the human in the form of a tricephalus. 



CHAPTER V. 

CIRCULATORY DISTURBANCES. 

Normal blood circulation is dependent upon the rate, rhythm 
and force of the heart, the caliber of the blood vessels and the 
resistance offered by them and the quantity and the quality of 
the blood. 

Variation of Heart Action. — A marked variation in the heart 
activity results in imperfect .circulation. Depressed \or dimin- 
ished heart actio^n is more common than increased heart action. 
Diminished functional activity is most frequently caused by in- 
flammation of the endocardium, myocardium, epicardium or per- 
icardium. Valvular stenosis and valvular insufficiency are the 
result of endocarditis. Myocarditis diminishes the activity of 
the heart and if the inflammation is long continued the muscle 
cells are destroyed and replaced by fibrous tissue thus per- 
manently impairing the force of the heart. Inflammation of the 
epicardium and pericardium may be accom^panied by volumin- 
ous exudation which distends the pericardial sac and produces 
sufficient pressure to hinder diastole, or the exudate may be- 
come coagulated and later organized attaching the sac to the 
surface of the heart and thus hindering cardiac systole. Cardiac 
activity may be diminished by the collection of fluid in the 
pleural cavity, malformed thoracic cavity, tumors, occlusion of 
coronary arteries, fatigue and thrombic formation upon the 
cardiac valves. Diminished cardiac activity results in a dimin- 
ished quantity of blood being sent out from the heart and an 
accumulation of waste products in the tissues. 

Increased functional activity of the heart is usually only tem- 
porary exceptiixg in those animals affected with cardiac com- 
pensatory hypertrophy. The most common cause of increased 
cardiac activity is reflex stimulation. Increased activity due 
to reflex stimulation may terminate in exhaustion and s3'ncope 
in a relatively short time. Increased functional activity, due 
to a cardiac compensatory hypertrophy resulting from increased 
resistance as in emphysema, chronic nephritis, etc., may result 
in permanent over action of the heart. 

Anatomical changes in the cardiac-structure, as hypertrophy, 
fatty degeneration, fragmentation, fibrous formation, or necrosis 

no 



CIRCULAR DISTURBANCES. Ill; 

may be evident when the functional activity of the heart is 
varied. 

Vascular Variations. — The amount of blood passing into or 
out of a given organ is determined by the caliber of the blood 
vessels, provided the heart action and general blood pressure , 
remain normal. Variations in the caliber of normal blood ves- 
sels depend primarily upon the response of the vessel muscu- 
lature to vaso-motor stimulation. Blood pressure is dependent 
upon the elasticity of the arteries and the force of the heart. In 
general, pathologic vascular variations are the result of, first, 
disturbed arterial elasticity ; second, the maintainance of the 
normal caliber of the vessels and ; third, the oermeability of the 
vascular walls. 

Arteriosclerosis is a condition in which the elasticity of the 
vessel walls is lessened or destroyed. In the production of 
arteriosclerosis there is vascular dilatation succeeded by suben- 
dothelial fibrous formation Avhich continues until the lumen uf 
the dilated vessel is reduced to its normal size. The hyper- 
plastic fibrous tissue may later become calcified. Sclerotic 
arteries are thick, stifif and nonelastic. Sclerosis is most com- 
mon in arteries although it occurs in veins. 

The vascular caliber may be diminished by muscular con- 
traction or by hypertrophied vessel walls. In animals affected 
w4th chronic nephritis there is contraction of the systemic 
arteries resulting in compensatory cardiac hypertrophy. Arterial 
constriction is also common in the peripheral vessels of animals 
afifected with carbon dioxide poisoning. Local diminution of 
vascular caliber may be produced by parietal thrombi. The 
vascular caliber may be increased by paralysis of the vaso- 
motor nerves a condition which is sometimes observed in ani- 
mals that have received injuries in the cervical region. 

Increased permeability of vessel w^alls usuallv results from 
insufficient nutriment to the vascular structures and occurs 
most frequently in small vessels, i. e., capillaries and venules. 
Increased permeability usually accompanies venous hyperemia 
although it may exist independent of variations in the quantity 
of blood. Thus oedema is common in hydremic individuals. 

Variations in Quantity and Quality of Blood. — The quantity 
of blood in a part is determined by the caliber of the supplying 
vessel and by the blood pressure. Acute general anemia re- 
sults in a diminished blood pressure which, if not corrected in 
a short time, terminates fatally. Chronic general anemia is 
accompanied by a slightly diminished blood pressure and a re- 
tarded blood current. 



112 VETERINARY PATHOLOGY. 

The most important variations in the quality of blood that 
concerns the student of general pathology are due to the varia- 
tions of the percentage of water contained. Hydremia is ac- 
companied bv disturbances of the renal function and by oedema. 
Anhydremia is productive of a slow weak pulse and the sec- 
ondary changes resulting therefrom. Excess of carbon dioxide 
or urea in the blood stimulates the vaso-constrictor nerves thus 
causing arterial contraction. 

Hemorrhagic diathesis or hemophilia is an inherited condi- 
tion in which there is little or no tendencv for coagulation of 
blood. The cause of this condition is the absence of some 
blood constituent essential to coagulation. 

HEMORRHAGE. 

DEFINITION. 
ETIOLOGY. 

Ruptured vessel. 

RJie.x-is Of diabrosis. 
Incyeased permeahility. 

Diapedesis. 
Predisposition ( hemophilia) . 
VARIETIES. 
Location. 
Tissue. 

Petechia (flea bite) pin point. 

Ecchymosis (over-ilozv) from pin point to size of dime. 
Suggillation {swelling) bruise. 
Eifusion. 

Hematoma (blood tumor). 
Infarction. 
Surface — Skin, mucous, membranC' serous membrane. 
Epistaxis. 
Hematemesis. 
Hemoptysis. 
Hematuria. 
Hematidrosis. 
Hematometra.. 
Hematocele. 
Metrorrhagia. 
Hemathorax. 
Heniocoelia. etc. 
Vessels. 

Cardium. 
Arteries. 
Veins. 
Capillaries. 
APPEARANCE. 
Macroscopic. 
Microscopic. 

Tissue hemorrhage. 
Clot. 
EFFECTS. 

Rate of outHozv. 

Location. 

Secondary chance of extravasate. 



CIRCULAR DISTURBANCES. 



113 



Hemorrhage is the escape of blood from a vessel, (capillary, 
vein, artery or heart.) 

Etiology. — Some animals are predisposed to hemorrhage 
(hemophilia). Hemorrhagic diathesis or hemophilia is an in- 
herited condition in which there is little or no tendency for 
coagulation of blood. The cause of this condition is the ab- 
sence of some blood constituent essential to coagulation 
or rupture of vessel wall, resulting from diseased vessels 
as ulceration, thus producing hemorrhage by diabrosis, or in 




o 



Fig-. 78. — Petechial hemorrhage, Kidney hog: cliclera lesion. 

a. Hemorrhagic area. c. Glomerulus engorged with blood, 

b. Normal kidney tubule. 



creased pressure and traumatism, thus producing hemorrhage 
by rJiexis. The permeability of the vessel walls may be suffi- 
ciently increased by pressure or disease so that hemorrhage 
takes place by diapcdcsis. The escaped blood, i. e., the ex- 
travasate, may flow upon the surface of the skin, serous or 
mucous membranes, or into the tissues. 

TISSUE HEMORRHAGES may vary greatly in amount and are 
designated by the following terms, petechia, ecchymosis, sug- 
gilation, effusion, infarction and hematoma. 

Pctechiae are small sharply defined hemorrhagic points and are 
probably caused by bacterial products in the blood. 



11 



VETERINARY PATHOLOGY 



Ecchymoses are hemmorrhagic spots larger than petechiae and 
less sharply defined caused by ruptured capillaries or precap- 
illaries. 

Suggillations and effusions are large indefinable hemorrhagic 
areas, caused by bruising which ruptures the small vessels. 

Hemorrhagic infarction is a hemorrhage into an anemic area. 
This is not a hemorrhage as ordinarily understood for the blood is 




Fig'. I'd. — Hematonia, caused by rupture of spur vein. 

within the vessels and escapes into the anemic area because of the 
diminished pressure. 

A hematoma is a circumscribed collection of extravasated 
blood in the tissues and is usually the result of hemorrhage 
from an artery. 

SURFACE HEMORRHAGE is designated according to its origin, thus: 

Epistaxis is hemorrhage from the nasal mucous membrane and 
is quite common in acute nasal glanders. 

Hemateinesis is hemorrhage from the stomach and is ob- 
served in animals poisoned with arsenic and those afflicted with 
gastric ulcer or gastric carcinoma. 

Hemoptysis is hemorrhage from the lungs. It may be the 
result of excessive exertic^n, abscess formation, tuberculosis, etc. 



CIRCULAR DISTURBANCES. 115 

Hematuria is hemorrhage into the urinary tract or bloody 
urine. The blood may escape from the kidney, and if so there 
will be tubular casts discernible on microscopic examination of 
the urine ; it may come from the ureter or bladder, and would 
then be thoroughly mixed with the urine ; or it may have its 
origin from the urethra and would not be mixed with the urine 
but would usually precede it. 

Hematidi'osis is hemorrhage! from the surface of the skin 
and is the so-called sweating of the blood and is caused by in- 
creased permeability of cutaneous capillaries. 

Entcrorrhagia is hemorrhage from the intestinal mucosa and 
may be differentiated from hematemesis by the appearance of 
the extravasate in the feces. The extravasate in hematemesis has 
the appearance of coffee bean grains in the feces while the en- 
tcrorrhagia extravasate retains the hemoglobin color and is not 
broken up into granules. (The coffee bean appearance of blood 
extravasated into the stomach is due to the action of the hydro- 
chloric acid of the gastric juice.) Enterorrhagia is caused by 
infection as in anthrax and by caustics. 

Heinatoinctra is hemorrhage from the uterine mucosa the 
extravasate beinof almost entirelv retained in the uterus. This 
is usually caused by improper removal of retained placenta. 

Metrorrhagia is hemorrhage from the uterine mucosa and the 
extravasate passes out of the uterus. Menstruation in the hu- 
man is an illustration of metrorrhagia. 

Hcmocoelia is hemorrhage into the peritoneal cavity and is 
caused by rupture of the peritoneum or some abdominal organ. 

Hemothorax is hemorrhage in the pleural cavity, and is 
caused by ruptured pleura as a result of fracture of a rib, etc. 

Hematocele is hemorrhage into the tunica vuginalis caz'ity. 
This may be the result of laceration or rupture of the tunica 
vaginalis testis. 

Effects. — The effects of a hemorrhage depend upon the 
quantity of blood lost and the location and secondary changes 
of the extravasate. In health the vascular system practically 
maintains a constant blood pressure by accomodating the 
capacity of the blood channels to the volume of the blood. 

The quantitv of blood that an animal may loose without be- 
ing seriously affected varies according to its age and health. 

The blood tissue of the horse has been estimated at from 
1-16 to 1-13 of the total body weight. One-tenth of the esti- 
mated total amount of blood in the body has been withdrawn 
from horses used in the production of anti-toxin once everv t'^/o 
weeks for from six to eight months without injurious results. 



1 10 VETERINARY PATHOLOGY. 

From Vs to Yi of the volume of the blood in the body may be 
withdrawn at once and the animal recover. Hemorrhage from 
a small vessel has little effect upon the welfare of the body for 
the quantity lost is immediately restored from the lymph and 
other fluids of the body. Thus there may be a constant hem- 
orrhage from the digital artery of the horse for twenty-four 
hours without injurious consequences. 

A sudden large loss of blood diminishes blood pressure and 
this results in imperfect action of the heart valves. The blood 
is churned back and forth, becomes mixed with air and this 
frothy mass accumulates beneath the valves and prevents their 
closure. 

Hemorrhage is serious when it occurs in the more delicate 
or the more highly organized tissues. Thus the amount of 
extravasate into the cerebrum may be very small and yet pro- 
duce sufficient disturbance to destroy life, while the same 
amount of extravasate into the muscles of the thigh, forearm, 
etc., would probably not be observed. 

The extravasation of blood into one of the body cavities, as 
the pleural or peritoneal cavity, will be partially absorbed as 
entire blood before it beecomes coagulated, the remaining un- 
absorbed portion will be in part disintegrated and carried out 
by the leucocytes and the remaining portion will finally be- 
come organized and remain as a mass of fibrous tissue. If the 
loss of blood is not sufficiently large to materially diminish the 
blood pressure and the extravasate remains free from infection 
there will be very little inconvenience from the hemorrhage; 
but if the extravasate becomes infected the outcome will be 
more serious. If the extravasate is into some important tissue 
the secondary changes will be of more consequence than when 
in the body cavities. 

There is a natural tendency for self arrest of hemorrhage, 
because, 1st, blood pressure is diminished during hemorrhage 
and thus coagulation is favored ; 2nd, the endothelium of the 
injured vessels becomes roughened and thus thrombic forma- 
tion is favored ; and 3rd, fibrinogen is liberated from vascular 
endothelium and thus the coagulation of the blood is favored. 



CIRCULAR DISTURBANCES. 1.17 

LYMPHORRHAGIA. 

DEFINITION. 

{Extent of lymphatic system). 

(Lymph transdate qiiantitx determined by blood pressure). 
ETIOLOGY. 

Ruptured vessel or space. 
LOCATION. 

Surface, because of lymph spaces and low pressure. 

Thoracic duct. 
APPEARANCE. 

Macroscopic. 

Microscopic. 
EFFECTS. 

Lymphorrhagia is the escape of lymph from ruptured 
lymphatic vessels. The lympathic system in general is the con- 
necting system between the blood capillaries and the jugular 
vein. In this system lymph is that portion of the blood which 
passes, through (or is secreted by), the capillary walls into the 
perivascular spaces and consists of plasma diluted, leucocytes, 
and usually contains considerable waste material. Lymph 
varies in its composition depending upon the source, location 
and condition of the surrounding tissue. The lymph of the 
lacteal system depends upon the kind of food-material di- 
gested and the length of time since its ingestion. 

Etiology. — Lymphorragia is the result of laceration or 
rupture of the lymphatic channels. Because of the low pressure 
within the lymphatic vessels, lymphorrhagia takes place only 
upon surfaces or into the body cavities. Lymphorrhagia onto a 
surface, if long continued, results in the so-called lymphatic 
fistula. Rupture of the abdominal portion of the thoracic duct 
accompanied by the escape of its contents into the peritoneal 
cavity produces the condition knowm as chylous ascites. 

Chylous ascites is differentiated from abdominal dropsy or 
ascites proper by examination of the accumulated fluid. The 
fluid of chylous ascites and lacteal fluid are practically identical 
in composition. Ascitic fluid proper is diluted lymph and con- 
tains no evidence of chyle or lacteal fluid. Lymphorrhagia may 
also occur into the pleural cavity as a result of the rupture of 
the thoracic portion of the thoracic duct. 

The effects of lymphorrhagia depend upon the extent, loca- 
tion and length of duration of the process. Extensive lymph- 
orrhagia from a large lymphatic vessel depletes the body be- 
cause of the loss of food substances, albumin, etc., in the lymph. 
Lymphorrhagia from the thoracic duct, especially into the 
peritoneal cavity, is serious because of the loss of food. 



118 VETERINARY PATHOLOGY. 

OEDEMA, DROPSY OR HYDROPS. 

DEFINITION. 
ETIOLOGY.- 

Increased production. 

Increased permeability (Cohnheiin.) 

Increased pressure. 
OBSTRUCTED OUTFLOW. 

Valvular insufficiency or stenosis (cardiac). 

Gravid uterus. 

Tumor ^ Abscess, Ligature, etc. 
LOCATION. 

Peritoneal cavity (ascites). 

Thoracic cavity (hydrothorax). 

Pericardial cavity (hydro pericardium). 

Arachnoid space (hydrocephalus external). 

Lateral ventricles (hydrocephalus internal). 

Tunica vaginalis cavity (hydrocele) . 

Subcutaneous lymph spaces (anasarca) (in legs only, stocking). 
APPEARANCE. 

Macroscopic. 

Microscopic. 
EFFECTS. 

Oedema, dropsy or hydrops is the accumulation and retention 
of lymph in the lymph vessels and spaces. Lymph is the 
conveyor of metabolic substances to and from all tissues of 
the body except those directly supplied by the blood capillaries. 
The quantity of lymph in the lymphatic channels is determined 
by the permeability of the capillary walls and the rapidity of 
lymphatic absorption. In health there is a balance between 
the transudation of lymph from the blood vessels and its 
absorption into the lymph vessels. In oedema there is either 
a larger amount of lymph transuded or a smaller amount 
absorbed. 

Etiology. — The causes of oedema may be : 

1. Increased transudation which may be caused by (A) 
Increased permeability (or secretory function) of the capillary 
walls, thus allowing an increased amount of fluid to escape 
from the blood. (B) Hyperemia: which produces an in- 
c'reased intracapillary pressure resulting in sufficient injury 
to the endothelial lining to allow an increased outflow of 
plasma. Passive hyperemia is more frequently associated with 
oedema than active hyperemia. Thus, tricuspid stenosis or 
tricuspid insufficiency is usually associated with general dropsy. 
"Stocking" is an oedema usually resulting from venous hyper- 



emia. 



i-;.^.: 



2. Obstructed outflozii of lymph. Swollen lymphatic glands, 
the result of inflammatory disturbances or neoplasms, and 



CIRCULAR DISTURBANCES. 



119 



external pressure hinder the passage of lymph and hence favor 
its accumulation. As the anastomoses of lymph channels is 
quite complete the obstruction of the outflow of lymph is a 
minor cause. 

Varieties of oedema accordino- to location are as follows: — • 




Fig-. 80. — Dog- with Ascites, a result of an hepatic tumor. 



Ascites: an abnormal accumulation of an oedematous fluid 
in the peritoneal cavity usually resulting from obstructed portal 
circulation. 

Hydrothorax, and abnormal accumulation of oedematous fluid 
in the pleural cavity or cavities. It is usually unilateral in the 
horse and is caused by obstruction of the internal thoracic vein. 

Hydropericardium : and abnormal accumulation of oedematous 
fluid in the pericardial -Sac. This variety is verv rare as a 
primary condition. It is caused from venous obstruction of 
cardiac vessels or vessels of the cardiac sac. 

Hydrocele: an abnormal accumulation of an oedematous 
fluid within the vaginal tunic, e. g., the so called "water seed", 
caused by adhesion of the vaginal tunic in the inguinal canal 
which is usually the result of improper castration. 

Hydrocephalus: an abnormal accumulation of oedematous 
fluid in the serous cavities of the brain or its meninges caused 
by venous hyperemia. Thus external hydrocephalus is an 



120 



VETERINARY PATHOLOGY. 



affection of the subarachnoidean spaces and internal hydroce- 
phalus an affection of the ventricles of the brain. 

Anasarca: an abnormal accumulation of oedematous fluid 
in the subcutaneous areolar tissue. 




Fig. 81. — Subcutaneous Oedema, caused by valvular iuaafficiency. 



Appearance. Macroscopic. — Oedema of the body cavities 
results in their distention and in the displacement of the normal 
cavity contents as a result of the accumulated fluid. The serous 
membrane becomes discolored. Oedematous fluid is thin, water- 
like, pale yellow, or colorless, contains less albumin and is less 
coagulable than either blood serum or inflammatory exudate. 
An oedematous tissue is swollen, flabby, soft and pits upon 



CIRCULAR DISTURBANCES. 121 

pressure, and if incised, a watery, pale straw colored fluid es- 
capes. 

Microscopic. — The intercellular spaces are increased in ex- 
tent, hence the cells are farther apart than normal and may be 
undergoing degeneration or atrophy, or be swollen and con- 
tain vacuoles. 

Effects. — The effects of oedema vary according to the causa- 
tive agent, the tissue involved, and the length of duration of 
the process. If the etiologic factor is capable of reproducing 
or increasing in quantity, as infectious agents (Bacillus of 
INIalignant Oedema), there is more extensive tissue destruction 
than when the oedema is produced by other agents. Oedema 
of the meninges of the brain or spinal cord may result in 
degeneration and destruction of the nerve cells and death of 
the diseased animal. O'n the other hand oedema of the sub- 
cutaneous tissues of the metacarpal or metatarsal region is of 
little consequence. Oedema of brief duration does not, as a 
rule, produce permanent injury to the involved tissue, but an 
oedema of long standing is of serious consequence because of 
the extensive hydropic infiltrations of the cells of the afifected 
tissue and because of the constant depletion of the system. 
Hydropic degeneration, thrombosis and necrosis are frequent 
sequellae of oedema. 



122 VETERINARY PATHOLOGY. 

THROMBOSIS. 

DEFINITION. 
ETIOLOGY. 

Injured endothelium. 

Mechanical — Artery forceps. 
Atheromatous degeneration. 
Insufficient nutrition. 
Foreign bodies — Parasites, etc. 
Retarded rate of blood How. 
Increased coagulability of blood. 
PROCESS OF FORMATION. 
LOCATION. 

Occurs in all vessels, more prevalent in veins and heart. 
VARIETIES OF THROMBI. 
Color. 
Red. 
White. 
Mixed. 
Extent. 
Partial. 

Lateral. 

Parietal {annular). 
Complete {obstructive). 
EXTENSION OF THROMBI. 
APPEARANCE. 

SECONDARY CHANGES OF THROMBI. 
Decolorization. 
Softening. 
Simple. 
Infective. 
Organization. 
Calcification. 
EFFECTS DEPEND UPON. 
Vessels obstructed. 
Secondary changes of thrombi. 

Thrombosis is the condition resulting from a coagulatiorj 
of blood within the vessels or heart during life. A thrombus 
is the coagulated blood within a living vessel. The accumula- 
tion and adhesion of leucocytes on the interior of vascular 
channels is also spoken of as a thrombus. The term thrombus 
should not be confused with a coagulum or a clot. A coagulum 
is coagulated blood within a vessel formed after death of the 
vessel wall, and a clot is coagulated blood formed outside of 
the vessel. 

Thrombosis is of quite common occurrence. It is occa- 
sionally a sequel of parturition, Thrombic formation of one 
or both of the iliac arteries of the horse is a demonstrated 
cause of lameness. Thrombo-embolic colic of the horse is 
caused by thrombosis of the anterior mesenteric artery. The 
appearance of ante-mortem clot is familiar to all post-mortem 
examination observers. Intravenous or intra-arterial injections 
are probably always succeeded bv thrombic formation at the- 



CIRCULAR DISTURBANCES. 123 

point of the injection, but the thrombi resulting therefrom are 
usually of little consequence. 

Etiology. — The coagulation of blood is a complex chemi- 
cal reaction and is not thoroughly understood. From the various 
investigations it may be concluded that three factors are essential 
in the coagulation of blood. 1st. There must be soluble albumins 
from which fibrin is derived. 2nd. Fibrin ferment (fibri^nogen) 
which is probably derived from leucocytes and blood plates. (It 
is probable that vascular endothelium may also liberate fibrinogen.) 
3rd. Soluble lime salts. The following are the most frequent im- 
mediate causes of thrombic formation. 

1. Injury of the vascular endothelium which may be caused 
by: (A) Mechanical interference, as torsion by artery forceps, 
or ligation: (B) Extension of disease from other portions of 
vessel walls, as atheromatous degeneration: (C) Insufficient 
nutrition the result of passive hyperemia: (D) Foreign bodies. 
Thrombic formation succeeding injury of the vascular endo- 
thelium is apparently a reaction on the part of the injured 
cells for protection and to prevent hemorrhage until the wound 
is repaired. Many thrombi are thus formed and later removed 
by phagocytes, without causing sufficient inconvenience to be 
clinically recognized. 

2. Retarded flozu of blood which may be caused by a weak 
heart or the relaxation of the blood vessels especially the veins. 
Frequently the so called "ante-mortem clot", which is a throm- 
bus, is observed in post-mortem examination of horses that 
have died of pneumonia, pleurisy, peritonitis and other ex- 
haustive diseases that are accompanied by a weak heart 
action. 

3. Variations in the composition of blood, as increased number 
of platelets, which increase its coagulability, (probably because of 
the production of fibrinogen), contamination with bacteria, etc. 

Process of Formation. — The process of formation varies ac- 
cording to the kind of thrombus formed. A red thrombus is 
formed when there is vascular obstruction and it is formed be- 
cause of the coagulation of the blood contained in the obstructed 
vessel. Coagulation in thrombic formation does not differ fromi 
extravascular coagulation, AVhite thrombi are formed as a result 
of leucocytic adhesion, and the deposition of the fibrin from the 
blood plasma on an injured internal vascular surface. The leu- 
cocytes and fibrin mav continue to accumulate until the vessel 
is obstructed. 

Location. — Thrombi form in the heart, veins, arteries, and 



124 VETERINARY PATHOLOGY. 

capillaries. They occur more frequently in the heart and veins 
because of the presence of valves. 

Varieties of Thrombi. — Thrombi may be classified on the 
basis of color and extents 

1. Color. Thrombi are variable in color according to their 
structure and may be red, white or mixed. A thrombus formed 
in a vessel in which there is complete stasis of blood will oc- 
cupy practically the entire vessel-lumen and be red. On the 
other hand a thrombus formed gradually by the deposition of 
fibrin upon a roughened endothelial surface of a blood vessel 
will be white. A mixed thrombus may be formed as a result 
of blood-stasis in a vessel in which there was a white throm- 
bus, or b}^ a red thrombus becoming partially detached from 
the vessel wall and contracting, thus allowing the blood to 
pass through the partially obstructed vessel and depositing 
fibrin (a white thrombus) upon the red thrombus. 

2. Extent. A thrombus may be complete or obstruutive, 
i. e., occupy the entire lumen of the vessels, or it may be partial. 
A partial thrombus may be lateral, i. e., be found along one side 
of a vessel. It may also be parietal, i. e., extend around the 
entire lumen of a vessel. 

Extension of Thrombi. — A thrombus may form las a plug 
in a vessel or may extend a considerable distance in the ves- 
sel, the extension usually being in the direction of the blood 
stream. Thus a bicuspid valve thrombus may extend, by 
continued deposit, out into the posterior aorta until it has 
reached the iliac arteries, or a thrombus arising in the metatar- 
sal region may extend up through the metatarsal and continu- 
ing veins until it reaches the posterior vena cava. The exten- 
sion may be the result of direct growth or deposit upon the 
original thrombus or it may be the result of fragments becom- 
ing detached (emboli) and floating in the blood stream until 
the}^ arrive at the junction of blood vessels too small to allow 
them to pass and so form secondary thrombi or produce embol- 
ism. 

Appearance of Thrombi.. — Macroscopic. — A red thrombus 
appears similar to a blood clot but is usually a little more dense. 
It is red, jelly-like and quite easily broken and may be partial 
or complete. A mixed thrombus is practically the same as the 
red except in color. A white thrombus is usually a little more 
brittle than the red, is yellowish white in color and if formed at 
different periods, strata may be observed. 

Microscopic. A red thrombus is practically identical with a 
blood clot, i. e., it is composed af fibrin in which white and red 



CIRCULAR DISTURBANCES. 



125 



blood cells are entangled. A white thrombus consists essentially of 
a mass of fibrin in which an occasional leucocyte of platelet 
may be found. 

Secondary Changes of Thrombi. — 1. Dccolorization. A red 
thrombus may become decolorized as a result of degenerative 



chang'es in the red bloods cells. 



The contained hemoglobin be- 




Fig-. Si\ — A Thrombus from the posterior aorta of a horse also a section of the 
] rsterior vena cava of a cow containing- a thrombus. 



ing liberated may in part be converted into other pigments and 
in part may be carried away by invading leucocytes. 

Softening. Thrombi, either red or white, are sometimes 
degenerated, disintegrated, absorbed and carried away as a 
result of the following: 

(A) Simple softening is a noninfective, degenerative pro- 
cess that begins in the center of the thrombic mass and con- 
sists of albuminous, granular or fatty degeneration. The spe- 
cific cause of the degeneration is not known but is no doubt 
the result of ferments. The degeneration extends from the 
'lenter until the entire thrombus is involved. The disinte- 



126 



VETERINARY PATHOLOGY. 



grated material may be carried away by leucocytes or may 
pass into the blood stream. 

(B) Infective softening is an infective degenerative process, 
the result of bacterial invasion into the thrombus. The source 
of bacteria, that infect thrombi, is usually from the blood or 
lymph. Suppuration or liquefaction is the resulting change. 










Fig. 83.— Red Thrombus, showing the fibrin, red cells and leucocjtts. 



The removal of the degenerative products may be accomplished 
either by the blood stream or by the leucocytes. The outcome 
of infective softening is likely to be much more serious than 
when simple softening occurs. 

3. Organization. If the thrombus does not undergo degen- 
eration it usually becomes organized, but it may become calci- 
fied. Very soon after a thrombus is formed the fibrin con- 
tracts as it does in the blood clot, thus reducing the size of the 
thrombus, and if it was a complete or occluding thrombus the 
reduction may be sufficient to allow the circulation to be re- 



CIRCULAR DISTURBANCES. 127 

established. The endothelium and the vasa vasorum of the 
contacting vessel proliferate and extend into the thrombus soon 
after the fibrin contracts, the vasa vasorum usually being of 
sufficient extent to produce complete vascularization of the 
thrombus. The proliferated endothelial cells become fibrous 
connective tissue cells and produce fibrous connective tissue 
which later contracts and thus reduces the size of the throm- 
bus. The dead and disintegrated tissue in the thrombus is car- 
ried away by leucocytes, thus reducing the size of the throm« 
bus still more. The contraction of the fibers usually continues 
until there is a mere cicatrix where there once existed an oc- 
cluding thrombus. (This is a favorable termination.) The or- 
ganization may result in the formation of an excessive amount 
of fibrous tissue which may practically occlude the vessel, and 
the vessel itself become a fibrous cord. 

4. Calcification of the thrombi in the human is quite com- 
mon, the calcified thrombi being called phleboliths and arteri- 
oliths, according to the vessel in which they occur. The same 
changes occur in thrombi of lower animals. 

Effects — The effects of thrombi depend upon the vessel 
in which it occurs and the nature of the thrombus. If it 
©ccurs in a terminal vessel the outcome will be different 
than if it occurs in a vessel having collateral branches. If the 
thrombus is occluding the outcome will be different than if it 
is parietal. A thrombus that is brittle or is easily detached will 
produce different results than one that is not easily broken 
and is adherent to the vessel wall. The general condition of 
the vessel wall is also a determining factor on the subsequent 
changes of a thrombus. The principle results are as follows : 

1. Obstructed circulation, which may be either partial or 
complete, depending upon the nature of the thrombus and of 
the vessel and the rapidity with which collateral circulation is 
established. Continued partial obstruction in veins favors 
hyperemia with its consequent oedema. Degeneration in ar- 
teries favors anemia and atrophy. Complete obstruction re- 
sults in necrosis with or without formation of infarcts. 

2. Production of embolism by fragments becoming de- 
tached and occluding smaller vessels. 

3. Formation of nezv blood 7;esseis. 



128 VETf:RlNARY PATHOLOGY. 

EMBOLISM. 

DEFINITION. 
SOURCE OF EMBOLI. 

Thromhic fragments. 

Cells, fat, leukemia, tumor, etc. 

Parasites. 

Air. 
LOCATION , where vessels branch. 
EFFECTS. 

Embolism is a condtion resulting from an obstruction of a 
blood vessel by a foreign body (embolus) that is suspended in 
the blood and is too large to pass through the vessel. An embo- 
lus is a foreign body in the blood such as air, sarcoma cells, 
etc. 

Source of Emboli. — Thromhic fragments. — Fragments from 
disintegrating thrombi float in the blood until they arrive at 
vessels that are too small to allow them to pass and there becom- 
ing impacted produce embolism. An entire thrombus may also 
become detached and float in the blood stream as an embolus 
v^hich, when impacted, would produce embolism. A thrombus in 
an .artery usually extends back to, and :sometimes beyond 
the first branch, the projection frequently becoming loosened and 
carried into the branch as an embolus. 

Abnormal ceils. — Leukemia is frequently accompanied by 
leukemic infarcts, a result of plugging of vessels by the enlarged 
leucocytes or leukemic cells. Metastatic sarcomata are the result 
of sarcomatous cells floating in the blood and becoming impacted 
in small vessels where they multiply, thus producing secondary 
tumors. Fat cells are a frequent cause of embolism especially 
in the human, after a fracture of a long bone in which the blood 
vessels are lacerated and fat cells from the marrow enter the 
blood stream. 

Parasites. — Embolism may be the result of animal parasites. 
The Strongylus armatus, in the larval stage is found in the 
blood vessels of the horse and frequently produces aneurisms 
of the anterior mesenteric artery. Here a thrombus forms, the 
fragments of which passing on as emboli thus produce obstruc- 
tions in the intestinal vessels which may result in thrombo- 
embolic colic. 

Vegetable microorganisms may cause embolism, thus bac- 
teria in the blood are emboli. Pyemia result from metastases 
of pyogenic organisms and pus. Apoplectic anthrax in sheep 
may be the result of emboli of Bacillus anthracis plugging the 
cerebral capillaries thus producing embolism. 

Air may act as an embolus and obstruct small vessels, or it 



ClRCULx\R DISTURBANCES. 



129 



may become mixed with the blood and become entangled in the 
cardiac valves, thus interfering with heart action (a horse was 
destroyed in four minutes by injecting air into the jugular 
vein). 

Location. — Embolism occurs most frequently in arteries and 
in the portal circulatory system. Venous emboli as a rule pass 
to the right side of the heart and into the pulm^onary arteries 
where they lodge. Fragments of thrombi from intestinal veins 
pass into the portal system and are lodged in the hepatic capil- 
laries thus producing embolism. Thrombic fragments from 



. ': i- - 




. ■,■ , 


...-' 


'■I 


■1 ' 




Si 

.■'"V 

. ', • 


L *^ * ' 


' 






h 






".''.'.1 








'■'■-M'i 


' '"■'/■■' 




('• '. 


■ '•'A 




Fig. 84. — Embolism. The embolus lodged at the point of division, of an artery. 



the pulmonary veins, bicuspid valve and semi-lunar valves pass 
into the arota and through its various branches and terminals 
as emboli and finally they occlude the containing vessel and thus 
produce embolism. Paradoxical embolism is the name applied 
to the condition resultino- from obstruction of an arterv with an 
embolus derived from the venous system and which has passed 
from the right side of the heart to the left through the foramen 
ovale. 



130 



VETERINARY PATHOLOGY 



In some rare instances it appears that an embolus travels 
in the direction opposite to the flow of blood and produces 
obstruction ; this is called retrograde embolism. 

Effect. — The results of embolism depend upon the composi- 
tion of the embolus, obstructed circulation and infarction. 




Fig. 85. — Anemic infarcts in the spleen. 
a. Infarcted areas due to emboli in capillaries supplying thein. 

Composition of the embolus. — Emboli composed of cells 
having the power to multiply, at the point of impaction (embol- 
ism) become secondary foci or metastases of the primary patho- 
logical condition, as metastatic sarcomata, leukemic infarctions, 
etc. Pathogenic bacterial emboli not only obstruct circulation, 
but also produce metastases of that disease as in necrobacillosis. 
anthrax, etc. Filarial emboli and emboli composed of fatty cells 
produce a mechanical effect only. Air emboli in small vessels 
are absorbed after a time. 



CIRCULAR DISTURBANCES. 131 

Obstructed circulation. — Obstructed circulation when produced 
by non-infective emboli will have the same ettects and terminations 
as the non-infective obstructive thrombi. 

Infarction. — Infarction is the process of obstructing a 
vessel with an embolus. The area supplied by the obstructed 
vessel is called an infarct. The area of infarction is determined 
by the region supplied by the occluded vessel and is usually 
wedge-shaped. An area supplied by an artery that has been in- 
farcted does not become bloodless at once because some of the 
blood remains in the vessels of the infarcted area and some 
may enter the periphery of the infarct through anastamosing 
capillaries and venules of adjacent regions. 

Infarcts may be anemic or hemorrhagic. 

An anemic infarct is one in which there is limited anasta- 
moses of venules and capillaries of contiguous areas. The blood 
remaining in the vessels of an anemic infarct soon becomes de- 
colorized and the area appears pale in color. Anemic infarcts 
usually undergo necrosis early because of the lack of nutrition. 
The type of necrosis is largely dependent upon the nature of 
the embolus. Infarcts produced by infectious emboli usually 
suppurate or putrefy and infarcts produced by non-infective em- 
boli may become liquified, absorbed and replaced with fibrous 
tissue or it may become caseated or calcified and surrounded by 
a fibrous capsule and persist for a long time. 

A hemorrhagic infarct is one in which there are anastamoses 
of the vessels of the infarct and the venules and capillaries 
of contiguous areas through wdiich blood passes and becomes 
stagnated in the affected area. Hemorrhagic infarcts may be- 
come decolorized, there mav be inflammation established around 
their periphery, or the blood and the involved tissue may be dis- 
integrated and absorbed. 

Infarcts may become cystic, caseous, calcareous, absorbed 
and substituted with fibrous tissue, or they may become infected 
and there may be abscess formation or gangrene. 

Infarction occurs most frequently in the kidney, spleen, brain, 
lung and less frequently in the heart, liver, retina, etc. 

Typical terminal arteries are common in the kidney and spleen 
and hence infarction frequently occurs in these organs. In 
the kidnev anemic infarcts are most common, hemorrhagic and 
anemic infarcts occur in the spleen. Cardiac infarction is not 
common and is usually caused by thrombosis of the coronary 
vessels. Cerebral anemic infarction occurs occasionally and the 
infarct usually undergoes simple softening, hemorrhagic cere- 
bral infarction is rare. 



13 J VETERINARY KA.THOLOGY. 

ISCHEMIA. 

DEFINITION. 
ETIOLOGY. 

Diminished calibre of supplying arteries. 
Stimulation of vaso constrictor nerves. 
Inhibition of vaso dilator nerves. 
Tonic spasms of vessel musculature. 
Occulsion of supplying arteries. 
Mechanical. 
Tumors. 
Thrombi, etc. 
Collateral hyperemia. 
APPEARANCE. 

Macroscopic, pale, flabby, lower temperature. 
Microscopic, cell degeneration, atrophy or necrosis. 
EFFECTS — Depend upon extent and duration and may be atrophy or 
necrosis. 

Anemia, as usually considered, is a condition in which there 
is either a dehciency in the quality or in the quantity of blood. 
The discussion of this theme will be found in special pathol- 
ogy- 

Ischemia is a condition in which there is insufficient or total 
absence of blood in a part of the body. 

Etiology. — Ischemia may be caused by influences that dimin- 
ish the calibre or occlude the vessels supplying blood to a part 
or by collateral hyperemia. The calibre of arteries may be 
diminished by contraction of the vessel musculature induced by 
low temperature, high temperature, drugs, etc., which stimulate 
the vaso-constrictor nerves, or inhibit the vaso-dilator nerves 
or cause tonic spasms of the vascular muscle. The supplying 
arteries may be occluded by mechanical pressure produced by 
bandages, ligatures, harness, collar, thronibi, emboli, neoplasms, 
tissue proliferations and tissue infiltrations. Ischemia in one 
part may be caused by hyperemia in a related part, because the 
blood of the entire body is easily contained in the vessels main- 
tained at the normal calibre, blood pressure causing an equal 
distribution of it ; and if the vessels of one area are increased in 
calibre, followed by an increased inflow of blood, the quantity of 
blood will be diminished in some part, thus a marked hypere- 
mia of the spleen is usually accompanied by ischemia of the 
stomach. It is possible for sufficient blood to collect in the ves- 
sels of the liver to drain the system to a sufficient extent that 
the animal would die of ischemia of the brain. 

Appearance.: — Macroscopic. — An ischemic tissue appears blood- 
less and is pale, flabby and of a lower temperature than 
the same tissue with a normal blood supply. If incised the tis- 
sue appears dry and there will be limited or no hemorrhage. 



JIRCULAR DISTCRBAXCES. 133 

Microscopic, the blood vessels are practically empty and die 
tissue cells are more or less shriveled as a result of insufficient 
moisture. 

Effects. — The outcome of ischemia is determined by the 
length of time it exists and the degree of completeness of the 
condition. Temporary, partial ischemia usually terminates in 
complete recovery. Continued partial ischemia is a frequent 
cause of atrophy. Complete absence of blood for a considerable 
time results in necrosis. 



HYPEREMIA. 

DEFINITION. 
ETIOLOGY. 

Enfeebled circidaiion. 

Mechanical interference. 
APPEARANCE. 

Macroscopic, bluish, cold clammy. 

Microscopic, engorged veins, degeneration. 
EFFECTS — Depend upon cause, duration, degree and location and may be 
fibrosis, oedema, thrombosis, necrosis and recovery. 

Hyperemia is a condition in which there is an increased 
quantity of blood in a part. The condition is practicallv local 
for an increased total amount of blood could not be retained in 
the general circulation w^ithout increasing the general blood 
pressure which would result in an increased production of lymph 
and hence diminish the volume of blood. Physiologic hyperemia 
is evident whenever an organ or part is active. Local patho- 
logic hyperemia may be passive (venous) or active (arterial). 

Passive or ^'Exous Hyperemia. 

Passive or venous hyperemia is a condition in which there 
is a normal quantity of blood constantly flowing into an organ 
or part, but a diminished quantity flowing out. An excess ot 
venous blood consequently accumulates in the part. 

Etiology. — Passive hyperemia is caused by enfeebled circu- 
lation due to weak heart, biscuspid and tricuspid insufficiency or 
stenosis, or diseased vessels and by pressure upon the outgoing 
vessels by ligatures, bandages, neoplasms, dislocations, fractures, 
etc. 

Appearance.. Macroscopic. — The afifected tissues are bluish 
in color and usually feel spongy, cold and moist when palpated. 

Microscopic. — A tissue affected with venous hyperemia has 
distended capillaries and venules, the lymph spaces are engorged 
with lymph and the cells are swollen and their protoplasm cloudy. 



134 VETERINARY PATHOLOGY. 

Effects. — The outcome of venous hyperemia depends upon 
the cause, degree, duration and organs affected. Thus venous 
hyperemia resulting from infective -,phlebitis is more serious 
than if caused by noninfectivev agencies. A venous hyperemia 
caused by complete obstruction of a vein is more likely to be 
fatal than one resulting from partial obstruction. Venous hy- 
peremia of short duration is usually of little consequence but, 
if long continued, it results in necrosis or fibrosis depending 
upon the degree of obstruction. 'Venous hyperemia of vital 
organs, as the brain or lungs, is more likely to have a fatal 
termination than if some less important structure as a muscle 
were involved. 

Therapeutic Venous Hyperemia properly produced results in 
(a), diminution of pain, probably because of the dilution of the 
irritating substances (b), destruction of bacteria, the. accumulated 
blood serum possessing strong, bactericidal properties (c), in- 
creased nutrition because of the increased amount of blood. 
Bier's hyperemia treatment of open joints by producing venous 
hyperemia illustrates this type. 

Pathologic Venous Hyperemia may result in fibrosis, oedema, 
thrombosis, necrosis, or recovery. A long continued slight ven- 
ous hyperemia usually results in 'fibrosis and is noted in 
the liver of animals affected with a slight tricuspid insuffi- 
ciency or stenosis. A marked venous hyperemia, but not 
caused by complete venous obstruction usually results in 
oedema, and is noted in the peritoneal cavity (ascites), in animals 
in which the portal circulation is partially obstructed. Venous 
hyperemia caused by complete obstruction results in throm- 
bosis and is observed in intussusception of the intestines. If other 
venous channels are unable to convey the blood from a part in 
which there is a complete venous thrombus, necrosis occurs as 
in strangulated herniae. Venous hyperemia of short duration, 
even though it is quite extensive, results in complete recovery if 
the cause is removed and the tissues are repaired. 



CIRCULAR DISTURBANCES. 



I6b 



ACTIVE OR ARTERIAL HYPEREMIA. 

ETIOLOGY. 

Increased calibre of arteries. 

Stimulation of vaso-dilator nerves. 
Inhibition of vaso-constrictor nerves. 
Paralysis of vessel musculature. 
Collateral ischemia. 
Diminished pressure. 
APPEARANCE. 

Macroscopic, red, hot, swollen. 
Microscopic, engorged arteries and capillaries. 
EFFECTS. 

Hypertrophy, hyperplasia, inflammation, recovery. 

Active or arterial hyperemia is a condition in which there 
is an increased inflow of blood to a part or organ without an 
equally increased outflow. 

Etiology. — Arterial hyperemia is caused by an increase 
in the calibre of the supplying arteries, by collateral ischemia 
and by diminished external pressure. The calibre of the supply- 
ing artery may be increased by stimulation of the vaso-dilator 
nerves, by heat, chemicals, etc., by inhibition of the vaso-con- 
strictor nerves, and by paralysis of the muscular tunic of the 
artery. 

The calibre of the surface vessels is in part the result of ex- 




Fig. 86. — Hyperemia, hemorrhage and oedema of intestine of a horse. 

a. Surface exudate. c. Area of oedema. 

b. Engorged vessels. d. Subsurface hemorrhage. 



136 



VETERI iX ARY PATHOLOGY. 



ternal pressure. If the external pressure is materially dimin- 
ished, there will be arterial hyperemia of the cutaneous arteries 
as is evidenced in hyperemia produced by cupping-. Collateral 
ischemia mav cause hyperemia of the related parts for the same 
reason that collateral hyperemia may cause ischemia. 

Appearance. — Macroscopic. — An arterial hyperemic part is 
scarlet red in color, usually feels dense, dry and has an increased 
temperature. If the tissues are incised, blood escapes freely. 




Microscopic. — Tissues affected with arterial hyperemia con- 
tain dilated arteries and capillaries, the lymph spaces are en- 
gorged with lymph, the tissue cells may be considerably swollen 
and diapedesis may be noted. 

Effects. — The eft'ects of arterial hyperemia depend upon 
the cause, degree, and duration and organs aft'ected. Arterial 
hyperemia caused by infective agencies is more serious than 
if causctl by other means. Arterial hyperemia of a sthenic 
type is usually succeeded by inflammation and asthenic hyper- 
emia may terminate in recovery. 



CIRCULAR DISTURBANCES. 137 

Arterial hyperemia of short duration is less serious than 
it would be if long continued, thus, active pulmonary hyper- 
aemia is occasionally aborted in the horse and such animals are 
usually ready for service in 24 to 48 hours, but if active pul- 
monary hyperemia continues for 24 hours it is succeeded by 
inflammation (pneumonia). 

Arterial hyperemia varies in different organs. Affections 
of the more highly organized structures are usually more seri- 
ous. 

Physiologic arterial hyperemia is a condition in which 
there is an increased amount of blood flowing into a tissue be- 
cause of increased physiologic demand, thus during gastric di- 
gestion an excess of blood passes to the stomach through the 
gastric arteries. 

Therapeutic arterial hyperemia, when properly produced 
in a diseased part, results in (a), diminished pain, (b). resorp- 
tion of inflammatory exudate, hemorrhagic extravasate, and 
oedematous transudate, (c) increased nutrition, thus by the al- 
ternate use of cold and hot applications an arterial hyperemia 
is produced and is of value in strained tendons, bruises, etc. 

Pathologic arterial hyperemia, may produce hypertrophy, 
hyperplasia and permanent arterial dilatation. Excessive de- 
velopment of a part (hypertrophy or hyperplasia) mav result 
from a long continued active hyperemia as in thickening of the 
skin as a result of continued application of blistering agents, 
but arterial hyperemia is as a rule of short duration for it 
usually terminates in recovery or is succeeded by inflammation. 



CHAPTER VI. 
INFLAMMATION. 

DEFINITION. ■ 

GENERAL CONSIDERATION OF STIMULI AND REACTIONS. i 

ETIOLOGY. \ 
Non-infective. 

Mechanic. .: 

Thermic. ' 

Electric. ; 

C hemic. : 

Infective. ' \ 

Nonsuppurative. \ 

FACTORS CONCERNED IN INFLAMMATION, (Phenomena.) ] 

Vascular. j 

Constriction of vessels. \ 

Dilatation of vessels. \ 

Acceleration of rate of blood How. ■ > 

Retardation of rate of blood How and leucocytic margination. -^ 

Oscillation of blood in the vessels and diapedesis. \ 
Stasis. 

Exudation. ' ! 

Exudate. ■ 

Composition. : 

Physic. ' 

C hemic. i 

Histologic. \ 

Varieties. \ 

Serous. 

Fibrinous. i 
Hemorrhagic. 
Factors determining quality and quantity. 

Cause of iniiammation. \ 
Condition of animal. 

Location of process arid of tissue affected. ' 

Significance of the exudate. ] 

Increased amount of nutrition to the affected part. — | 

Dilutes, counteracts, neutralises or destroys the irritant. ] 

Circumscribes the inflammatory process. 

Chemotaxis. : 

Phagocytosis. j 

THE SIGNS OF INFLAMMATION. \ 

Redness \ 

Swelling. \ 

Increased temperature. ■ 

Pain. ; 

Im.paired function. i 

EFFECTS UPON THE TISSUE INVOLVED. j 

Degeneration. j 

Parenchymatous. \ 

Fatty. \ 

Mucoid. ■ 

Serous. \ 

Amyloid. { 

Hyaline. \ 

Necrosis. \ 

Regeneration or proliferation. , 

138 I 



INFLAMMATION. 139 

THE KINDS OF INFLAMMATION. 
Etiology. 
Simple. 
Infective. 

Nonsuppurative. 
Suppurative. 
Surface. 
Sub-surface. 
Exudate. 
Serous. 
Fibrinous. 
Hemorrhagic. 
Tissue. 

Parenchymatous. 

Interstitial. ".'. 

Time, activity and results. -_ 

Acute. 
Chronic. 
Miscellaneous. ' ■/. 

Catarrhal. 
Purulent. 
Ulcerative. 
Vesicular. 
Pustular, 
Proliferative. 
Specific. 
TERMINATION. 

Resolution. 
Tissue proliferation. 
Dissolution. 
CONCLUSIONS. 

Inflammation is a name applied to a group of pathologic 
processes including circulatory disturbances, retrogressive and 
progressive tissue changes. The term inflammation is diflicult 
to define because of the several factors entering into the process 
and of the variation of each factor. It may be defined as the 
reaction of a living animal tissue to an irritant. 

A stimulus is anything that produces action in a living tis- 
sue. An irritant is anything that produces excessive stimulation 
in a responsive tissue. Stimuli and irritants differ only in 
degree. Mild friction of the skin is a stimulus to that structure. 
When the friction is intensified and the cutaneous function is 
overstimulated the friction becomes an irritant. All living tis- 
sues respond to stimuli and likewise to irritants. The response 
or reaction of a living tissue to an irritant, i. e. excessive tissue 
stimulation, accompanied by circulatory disturbances and by 
destructive or proliferative tissue changes, constitutes the pro- 
cess known as inflammation. The general phenomena of in- 
flammation will be better understood if some preliminary con- 
siderations of the reaction to stimuli are first discussed. 

General Consideration of Stimuli and Reactions. — It is a 



140 VETERINARY PATHOLOGY. 

well known fact that all living things (organisms) respond to 
stimuli. A stimulus is that which excites or produces a tem- 
porary increased vital action, or it is any substance or agent 
capable of producing activity in a living tissue or producing 
an impression upon a sensory organ. The extent or degree 
of response to a stimulus is directly proportional to the organi- 
zation and complexity of the tissue and especially those tissues 
which are : (a) capable of being stimulated ; (b) capable of trans- 
mitting an impulse ; and (c) capable of interpreting the impres- 
sions produced by the impulse. The following discussion of 
response to stimuli is confined to animal tissues because inflam- 
mation affects animals only. 

Protozoa, although of the simpliest structure, consisting of 
a single cell, respond to the various stimuli. They respond to 
light. Thus, if a portion of a cover glass preparation of living 
amoebae be exposed to intense light, the amoebae in the 
lighted area will, in a short time, become restless and begin 
to move about and will finally move away from the area of 
light. By a specially arranged hot stage, so that there are areas 
of different temperature, amoebae will be observed to ac- 
cumulate in the areas of favorable temperature and emigrate 
from those of unfavorable temperature. That is, they respond 
to or are responsive to thermic stimuli. In a similar way 
amoebae respond to various chemical stimuli. If a drop of acid 
be so placed that it will slowly diffuse into the water or fluid 
in which the amoebae are being studied, they will move away 
from the acid. If an amoeba be divided by mechanical means 
so that one segment contains the entire nucleus and the other 
segment has no nucleus, it will be observed that the nucleated 
segment responds to the stimulus by regenerating tissus to re- 
place the nonnucleated segment which was removed. On the 
other hand, the nonnucleated segment of the amoeba may 
survive the shock of separation, but soon begins to degenerate 
and finally dies. Thus is shown the response of living struc- 
ture to photic, thermic, chemic and mechanic stimuli. 

If more complex animals be considered there will be ob- 
served a similar response to stimuli. Thus, the hydra responds 
to the various kinds of stimuli and has a remarkable power of 
regeneration of tissues. Vermes are very responsive to stimuli 
and all observers have noticed that when an angle-worm is 
cut in two both ends will crawl away. Vermes are among the 
lowest forms of animals that possess cells corresponding to 
white corpuscles or leucocytes of higher animals. These cells 
are observed to emigrate to the point of injury or to surround 



INFLAMMATION. 141 

the foreign bodies or substances that are experimentally in- 
troduced into the bodies of vermes. This reaction is analogous 
to the reaction of the mammalian leucocytes. 

The discussion so far, has been with reference to animals 
that possess no blood or vascular systems, or at least only in 
a rudimentary form. 

Vertebrates are more highly organized and are consequently 
more responsive to stimuli than invertebrates. Mammalia arc 
the most complex in structure of all animals and they are like- 
wise most responsive to stimuli. 

The mammalian cornea is a nonvascular structure being 
composed of fused layers of fibres arranged parallel to the sur- 
face. Between the layers of fibres connective tissue cells and 
lymph spaces are found but no nerves. The cornea is covered 
externally by the conjunctiva. If the cornea be irritated there 
will be a reaction, the extent of which depends upon the in- 
tensity of the irritant. A puncture of the cornea with a sterile 
needle produces the following reaction or tissue changes ; (a) 
within a few hours after the injury the affected area appears 
swollen and the cells that were punctured begin to degenerate 
while the uninjured cells imimediately surrounding the needle 
puncture become tumefied and vacuolated ; (b) from twenty to 
thirty hours after the puncture, wandering cells appear in and 
around the injured area, and as the cornea is nonvascular they 
must be migratory connective tissue cells ; (c) by the third 
or fourth day the punctured cells will have been removed, by 
solution or otherwise, from the affected areas. Those cells sur- 
rounding the injury will have divided by mitosis, the newly 
formed cells replacing those that were destroyed and the 
wandering cells will have migrated from the injured focus. 
(The destroyed epithelial cells of the conjunctiva are replaced 
by those next to the injtiry). 

If sterile iron dust, or other insoluble granular material is 
aseptically introduced into the cornea, a reaction, as described 
above, will take place, and, in addition, the migratory connec- 
tive tissue cells will ingest or incorporate the introduced par- 
ticles and carry them out of the injured focus. 

When the cornea is injured more severely, as by the ap- 
plication of a caustic solution (irritant), in addition to the 
above reaction, a migration of leucocytes from the marginal 
corneal vessels usually occurs within thirty hours. Some of 
the invading leucocytes become destroyed and some of them 
may multiply, but they usually all disappear from the point of 
mjury within from forty to fifty hours. The length of time 



142 VETERINARY PATHOLOGY. 

necessary for repair of such an injury is variable according to 
the extent of the injury and the readiness of response of the 
tissue. 

In vascular tissue the follow^ing reaction occurs. An asep- 
tic cutaneous incision unites almost immediately if the wound 
margins are placed and maintained in exact apposition. The 
tumefaction is slight because of the limited extravasate from 
the severed vessels. There is a slight exudate v^hich coagu- 
lates and cements the margins or lips of the wound. In a 
microscopic section through such a wound some cells are found 
destroyed and others injured. The cells bordering such an in- 
jury sometimes increase in size to such an extent that they 
project into the cement between the two incised surfaces. Wan- 
dering cells and leucocytes in varying numbers appear through- 
out the entire injured area. The cement (exudate) and the de- 
generated and necrotic marginal cells are later absorbed. The 
cells bordering the incision multiply by direct cell division, the 
newly formed cells replacing those destroyed. New capillaries 
extend through the newly formed tissue. Finally the leucocytes 
emigrate and disappear from the injured area. 

In a more extensive injury, such as a gaping wound that 
later becomes infected, a more complex reaction is observed. 
The following changes take place during the first twenty-four 
hours after an injury of this nature is inflicted. There is hem- 
orrhage, the extent of which depends upon the size of the ves- 
sels severed and the gaping of the wound. The extravasated 
blood accumulates in the wound and also infiltrates the ad- 
jacent tissues. The injury (irritation) causes hyperemia, es- 
pecially of the arterioles, resulting in engorgement of the capil- 
laries. From the engorged and dilated capillaries there is 
marked exudation. The exudate escapes upon the wound sur- 
face and infiltrates the tissues of the injured area. The ac- 
cumulation of the hemorrhagic extravasate and the inflam- 
matory exudate plus the increased size of the vessels (hyper- 
emia) tumefies or swells the injured area. There is an ac- 
cumulation of mononuclear leucocytes or wandering connec- 
tive tissue cells in the injured tissue and an immigration of 
polymorphonuclear leucocytes. Many cells are destroyed out- 
right by the injury or by the action of infectious bacteria. 
Those cells bordering the destroyed cells are injured and be- 
come tumefied and may later undergo necrosis. The cells, es- 
pecially the connective tissue cells located peripherally to the 
injured cells, become enlarged and multiply by indirect cell di- 
vision. The injured cells are repaired and the newly formed 



INFLAMMATION. 143 

cells are massed together and project outward thus replacing 
the destroyed cells. 

The discharge from such a wound after twenty hours con- 
sists of serum, shreds and fragments of necrotic tissue, dead 
cells (especially leucocytes) and a variety of microorganisms. 

The reaction in the above case consists of circulatory dis- 
turbances, degeneration, necrosis, and regeneration of tissues. 

Etiology. — The exciting causes of inflammation may act 
from within the body, hematogenous or lymphogenous, or from 
without, i. e., extraneous as burning, etc. They may produce their 
action by direct contact upon surfaces of the body as from a 
blistering agent externally applied, or, by contact internally, as 
from arsenic. They may produce their effect while being ex- 
creted, as in the production of nephritis by cantharides or tur- 
pentine. Some harmless agents may become irritants as the 
result of chemic change produced by some of the body juices 
or fluids (lysins). 

The causes of inflammation mav be divided into two gen- 
eral classes, non-infectious and infectious. 

NoN-iNFECTious. — The non-infectious causative factors are not 
as active in producing inflammatory disturbances as the in- 
fectious agencies, but they are of some importance and should 
not be overlooked. Some have positively stated that "There 
is no inflammation without infection." Reasonable interpreta- 
tions of clinical and experimental observations supply suffi- 
cient evidence that there is inflammation without infection. 
The following are the principal non-infectious causes of in- 
flammation. 

Mechanic or traumatic. — Surgical wounds which heal by 
primary union are undisputed examples of mechanically pro- 
duced inflammation. The reaction taking place in an aseptic 
incision consists in cell-destruction, slight circulatory disturb- 
ances, leucocytic immigration and regeneration of tissue. Such 
a reaction is typical of inflammation and the affected area is 
devoid of any infection. A sterile needle introduced into a 
tissue, the surface of which is aseptic, produces a reaction 
identical to the reaction observed in primary union of tissue. 
Mechanic or traumatic causes of inflammation may produce, or 
cause to be produced in the injured cells, chemic substances 
that are responsible for the reaction. 

Thermic. — A temporary exposure to a high or low tem- 
perature is sufficiently irritating to produce a marked inflam- 
mation. Let those doubting this statement take the chimney 
from a lighted lamp and hold it in the hand for one minute and 



144 VETERINARY PATHOLOGY. 

they will acknowledge that heat produces all the symptomatic 
evidences of inflammation and there is no infection. The prin- 
ciple object in the use of the thermo-cautery is to produce or 
establish inflammation. A thermo-cautery, or any severe burn, 
produces tissue necrosis, as well as the destruction of bacteria 
in that area (sterilization), and an inflammatory zone is im- 
mediately established around the necrotic tissue which is sterile 
and may remain free from infection. 

A short exposure to an extremely low temperature produces 
an inflammation. If the exposure is of long duration necrosis 
is likely to occur. "Chilblains" is an inflammation resulting 
from temporary exposure to a low temperature. Sloughing 
following freezing of calves' ears, pigs' tails and cocks' combs 
are familiar examples of necrosis resulting from long exposure 
to extremely low temperature. An inflammatory zone is es- 
tablished around necrotic areas produced by freezing similar 
to the inflammatory zone observed around necrotic areas pro- 
duced by burning. Thermic variations may produce chemic 
substances in injured tissues which are sufficiently irritating to 
establish inflammation. 

Electric. — It is common knowledge that electricity causes 
inflammation. Animals injured by lightning usually show evi- 
dences of cutaneous inflammation. In cities animals as well as 
men frequently contact wires charged with powerful electric 
currents and receive local injuries that are usually inflammatory 
in their nature. 

Chemic. — There are many chemicals that are irritants. A 
number of them are used as therapeutic agents when irritants 
are indicated. Mineral acids, caustic alkalies, mercury salts 
and arsenic are some examples of chemic agents that produce 
inflammation when applied in dilute solutions, and necrosis 
when applied in more concentrated form. A 10 per cent solu- 
tion of nitric acid applied to the skin for a very short time pro- 
duces inflammation. Inflammatory symptoms following the 
nitric acid application appear immediately ; and, as the acid is 
a disinfectant, the inflammation cannot be the result of infec- 
tion. In animals poisoned by any of the mineral poisons there 
may always be observed an inflammation in the mucosa of the 
alimentary tract more extensive than could have been produced 
by infection in the limited time of action. 

Many reptiles, bees, wasps, and ants introduce chemic sub- 
stances into animal tissues that are extremely injurious and es- 
tablish inflammation of very rapid evolution. 

Infectious or vital agencies are the most important etiologic 



INFLAMMATION. 145 

factors in the production of inflammation because they are the 
most frequent offenders. Infection usuaMy produce inflam- 
matory disturbances through the action of chemic substances 
elaborated by the infecting micro-organisms, as metabolic pro- 
ducts. The infection may be local and produce localized in- 
flammation as in a superficial abscess and in coccidiosis. The 
elaborated chemic substances may be absorbed from the local- 
ized infection and produce inflammation elsewhere in the body. 
Infection may be general and produce conditions similar to in- 
flammation in practically all the tissues of the body as in gen- 
eralized anthrax. However, the term inflammation is usually 
confined to local disturbances. The extent of irritation pro- 
duced by any infecting organism is dependent upon the virul- 
ency of the given organism and the resistance of the infected 
animal. Thus, infection with Streptococcus pyogenes equi may 
produce pyemia in one animal and only a local abscess in an- 
other. Again, some bacteria, as the anthrax bacilli, may pro- 
duce septicaemia in one animal and localized inflammation in 
another. A concise etiological classification of inflammation 
produced by living organisms is impossible because of variations 
both in the virulency of the organisms and in the resistance of 
the tissues. Animal parasites are of considerable consequence 
in the production of inflammation. They may produce inflam- 
mation by mechanical interference, as the Echinorychus '^:igs.s 
which inserts its barbed proboscis into the intestinal mucosa 
thus injuring the tissue as well as opening an avenue for the 
entrance of various bacteria. The Trichina spiralis bv perfor- 
ating the intestinal wall and by burrowing in the muscular 
tissue produces sufficient irritation to establish inflammation, 
the results of which are evidenced on microscopic examina- 
tion of a lesion. It has been suggested that the etiological 
factor of rabies is an animal parasite ; the round-celled infil- 
tration of the ganglionic nerve cells and perivascular spaces 
having marked characteristics of the lesions of inflammation. 
Psorospermosis, a condition resulting from psorospermic in- 
festation, is inflammatory in its character. 

In a general way infective inflammations mav be discussed 
as non-suppurative and suppurative. 

The non-suppurative infective inflammations are those in- 
flammatory disturbances in w^hich there is no purulent fluid or 
pus produced. As examples the folloAving may be cited — septic 
infection succeeding nail pricks in horses feet ; blackleg in 
calves caused by the Bacillus anthracis symptomaticus. (Sar- 



146 VETERINARY PATHOLOGY. 

cophysematous bovis) ; malignant oedema caused by the Bacil- 
lus of malignant oedema. 

Suppurative infective inflammation is characterized by the 
formation of pus. The causative bacterial agents of suppura- 
tion are designated as pyogenic bacteria or pyobacteria. The 
following are the most important bacteria of this class : 

Staphylococcus pyogenes aureus. 

Staphylococcus pyogenes albus. 

Staphylococcus pyogenes citreus. 

Strepto-coccus pyogenes 

Baccillus pyocyaneus. 
Factors Concerned in Inflammation. — The animal body is 
an intricate mechanism composed of different tissues in various 
combinations. The phenomena of inflammation are the changes 
that take place in the tissues plus the conditions resulting from 
those tissue changes, thus including all the changes taking place 
in the inflammatory focus. The following are the most impor- 
tant. 

Vascular disturbances. — These are universally present in 
animals possessing a vascular system, but inflammation, or a 
condition analagous to it, occurs in the tissues of animals that 
have no vascular system, and in nonvascular tissues of animals 
that have a vascular system. Hence vascular changes are not 
essential in the process. The vascular changes are dependent 
upon nervous influence, because the calibre of blood vessels, 
especially arteries, is controlled by vasomotor nerves, i. e., vaso- 
dilators and vaso-constrictors ; stimulation of the former produc- 
ing dilatation, of the latter constriction of the vessel. Inflam- 
matory areas become necrotic when dilatation of the supplying 
arteries and arterioles is inhibited. In experiments in which 
dilatation of the arterioles takes place the inflammatory pro- 
cess is limited and usually terminates in recovery in a short 
time. Necrosis usually succeeds inflammation in tissues in 
which communications of the vasomotor nerves have been de- 
stroyed. For example, the cubital nerve in the horse probably 
contains the vasomotor fibres that innervate the vessels of the 
foot and the median nerve the sensitive fibres that innervate 
the pedal structures. Median neurectomy is not succeeded by 
vascular disturbances, but cubital neurectomy is frequently 
succeeded by vascular disturbances and excessive exudation 
that terminates in necrosis followed b}^ sloughing of the hoof. 

The following vascular changes occur in an inflammatory 
focus and in the order designated : 

Decreased calibre of the supplying arteries and arterioles. 



INFLAMMATION 



147 



Temporary contraction of arteries is the first result of the ap- 
plication of an irritant. The cause of the constriction of the 
arteries is a spasmodic contraction of the musculature of the 
vessels. This is succeeded by a marked arterial dilatation. 

Dilatation of the arteries and arterioles. The response to 
stimuli on the arteries is rapid and always active, in veins slow 
and usually passive, in capillaries either rapid or slow but al- 
ways passive. Dilatation of vessels in an inflamed area is 
caused by stimulation of the vaso-dilators or inhibition of the 




o 2 D o^ o o 



o o 



# 



> c 

o 

^o"o^o''o^Q-o^o>~6o o-oo~,^,3^0o^ooSo:^"6^'15'0^^ 0-0-00:0-00-00- o c •■ ^ 





Fig. 88. — Blood vessel, showing Corpuscles occupying central portion of streani, 

tynical of normal circulation. 



vaso-constrictors. An increase in the calibre of the arteries 
results in an increased amount of blood flowing through them 
and into the capillaries. The increased amount of blood in the 
capillaries mechanically increases their calibre and also in- 
creases the amount of blood which enters the related veins and 
results in a dilatation of them. By increasing the lumen of n 
vessel the resistance to the flowing contents is correspondingly 
diminished and this results in a temporary acceleration of the 
rate of blood flow. 

Acceleration of the rate of flow of the blood. The cor- 
puscles occupy the axial, or central part of the stream as in 
the normal circulating blood. The arterial dilatation plus the 
acceleration of the blood flow constitute the essential factors m 
active hyperemia. 



148 



VETERINARY PATHOLOGY. 



Retardation of the rate of flow. — A long continued dilata-^ 
tion of a vessel results in injury especially to the endothelial 
lining. The injured endothelial cells become sv^^ollen, rough- 
ened and sticky. The leucocytes begin to appear in the peri- 
pheral portion of the stream, probably because of the libera- 
tion of some chemic substance by the endothelium that exerts 
a partial chemotactic action upon the leucocytes. They roll, 




Fi£ 



89. — Dilated blood vessel showing- corpuscles spread throughout the entire 
lumen typical of first stages of hyperemia. 



tumble, and creep along over the swollen endothelial cells and 
finally adhere to their roughened surfaces. The continued at- 
tachment of leucocytes to the endothelium diminishes the cali- 
bre of the vessel and increases the resistance thus retarding 
the rate of blood flow. 

Oscillation. — The resistance of the flowing blood, due to the 
roughened endothelium of the vessels and accumulation of 
leucocytes becomes so increased that the propelling force is 
momentarily overcome. The blood in the engorged capillaries 
and arteries may temporarily cease flowing or it may flow 
toward the heart, i. e. in the reverse direction during the dias- 
tolic periods. This to and fro movement is termed oscillation. 



INFLAMMATION. 



149 



Stasis. — The resistance may become greater than the pro- 
pelling force and the circulation cease for a varying period of 
time. This condition is denominated stasis. 

Exudation. — Varying quantities of the fluid and of the cell- 
ular constituents of the blood pass through the vessels nor- 
mally and an increased quantity escapes through during in- 
flammation. The portion of the blood that escapes through the 
blood vessels is called exudate. The passing of the exudate 




S>'^SC^»S''''c*r — '^■'^i^r'^jti^f. ■ 






iOCOOOO 



w --.o/^^P O^ ^ S(^0 KS^oCo S^^C O OOOX o 



o 






ic 



o <^o 



.CO' 



o 






C^o C .-r> C S^c:; o c C-C C-- ' 



c c c cs'^o 



-„Q^Q - 



(-< 7-( o o c o _^ 




Fig. 90. — Blood vtssel showing margination of leucocytes typical of the first stages 

of inflammation. 



through the vessel wall is termed exudation. It is still unde- 
termined whether the normal tissue lymph is a secretory pro- 
duct of the capillary endothelium or is produced by such ph3'si- 
cal processes as diffusion or filtration. The source of the in- 
flammatory exudate is no doubt, the same as the source cf nor- 
mal tissue lymph. Exudation is a result of the vascular dis- 
turbances. 

It has been previously stated that in normal circulatory 
blood the corpuscles occupy the axial stream and the plasma the 



150 



VETERINARY PATHOLOGY. 



peripheral stream. The corpuscles occupy the axial stream 
because they have a greater specific gravity than the plasma. 
Why the leucocytes enter the peripheral or plasmatic stream in 
inflammation has not been clearly determined, but it is probable 
that this margination is a result of chemotactic influences. 
After the leucocytes become marginated they pass through the 
vessel wall as follows : Small protoplasmic processes extend 
and project through the vessel wall. These processes gradually 
increase in size until the entire leucocyte has, by protoplasmic 
extension, passed through. The leucocytes usually pass be- 
tween the endothelial cells but they may pass directly through 



Q ^ 






o -^ 
o 




B'ig-, 91. — Blood vessel showing diapedesis of leucocytes typical of the exudative 

stage of inflammation. 



them. The exudation of erythrocytes is passive, the cells being 
forced through the vessel wall by pressure. To recapitulate: 
fluid exudation is either a physical process, such as filtration, or 
a physiologic process, a secretion ; leucocytic exudation is a 
physiologic process depending largely upon the chemic influ- 
ences of the adjacent tissues, i. e., chemotaxis ; exudation of 
erythrocytes is a physical process resulting from intravascular 
pressure plus diminished resistance of the vessel wall. 

Exudate. 1. Composition. — Inflammatory exudate contains 
varying quantities of cells suspended in a fluid (plasma, tissue 
juice, etc). The fluid part of the exudate contains proteids 
(serum albumin and serum globulin) in excess of normal plasma. 
It has a specific gravity of 1018 or more. The quantity of pro- 
teid is directly proportional to the severity of the process and 



INFLAMMATIOX, 



151 



is never less than 4 per cent and frequently as much as 6 per 
cent. It usually coagulates readily if withdrawn from the in- 
flammatory tissues. The coagulability of inflammatory exudate 
is so constant that it may be used in differentiating inflamma- 
tion from oedema. The exudate is usually acid in reaction. 
The fluid portion of the exudate is similar to the blood plasma 
with the exception of the varying percentage of proteids, and 
the presence of some other soluble substances. Leucocytes are 
the principal cellular elements found in the exudate, erythrocytes 
occurring only in certain inflammatory conditions, such as 
croupus pneumonia. 

The following types of leucocytes are especially concerned 
in inflammation; polymorphonuclear, lymphocytes small and 
large. Polymorphonuclear leucocytes w4th neutrophile gran- 
ules are the type most frequently found in an area affected 
with acute inflammation, providing the causative irritant was 
not too severe. About 70 per cent of the leucocytes present are 
of this type. These cells appear in the aff'ected area in the be- 
gining of the process. They have the power of amoeboid 
movement and may emigrate from the blood and lymph vessels 
independently of the fluid exudate. These cells possess phago- 
cytic properties and probably produce and liberate antitoxic and 
bactericidal substances. They are the pus cells and constitute 
the bulk of the exiidate in suppuration. These cells may be 
destroyed and disintegrated in the field of action or when the 
inflammatory process ceases they may migrate from the in- 
jured area and reenter the lymph or blood vessels. They do 
not become formative cells and never produce new tissue. 

Eosinophylic leucocytes, (polymorphonuclear leucocytes hav- 









Fig. 92. — Types of cells in inflammatory exudates. 

1. Lymphocyte. 4_5. Polymorphonuclear leucocytes. 
3. Transitional leucocyte. g. 

2. Mononuclear leucocyte. 



Endothelial cells from lining of an artery. 



152 VETERINARY PATHOLOGY. 

ing acidophile granules), appear early in an inflamed area. 
They are usually quite limited in number except in localized 
inflammation induced by animal parasites. There are frequently 
observed in the liver, kidney, and other tissues, foci composed 
of a mass of eosinophiles and appearing as inflammatory cen- 
ters. These eosinophilic inflammatory foci are probably the re- 
sult of invasion of animal parasites. Eosinophiles are abundant 
in the lesions of bursattae and in epizootic lymphangitis. Their 
origin is, so far as has been determined, from the blood, the 
lymph and tissue spaces indirectly, and the bone marrow di- 
rectly. The specific action of these cells in inflammation is 
not known. They do not aid in the formation of new tissues. 
Mast cells or polymorphonuclear leucocytes with basophile 
granules are observed in subacute inflammation (Adamij. 
Their origin is from bone marrow. Their nuclei apparently 
become disintegrated in inflamed tissue. The significance of 
these cells has not been determined. 

Lymphocytic invasion of the afifected areas and an excess of 
them in the blood characterize some of the slow p'oine or 
chronic inflammatory processes such as tuberculosis and ac- 
tinomycosis. These cells also appear in aft'ected tissues in ihe 
later stage of acute inflammation but are never very abundant. 
They may have their origin from the blood, the lymph and 
from adjacent lymphoid tissue. The large lymphocytes may 
have their origin from the small lymphocytes. Lymphocytes 
have a very limited power of amoeboid movement. They have 
never been observed to ingest bacteria although they may in- 
corporate fragments of destroyed tissue cells or other inert sub- 
stances. These cells may partake in the formation of new tis- 
sue but this has not yet been positively determined. 

Cells other than leucocytes are sometimes observed in in- 
flammatory foci. Endothelial cells, wandering connective tis- 
sue cells, giant cells, and red blood corpuscles may be present in 
inflamed areas. 

Endothelial cells are especially evident in serous membranes 
aft'ected with inflammation. They appear later in the process 
than either polymorphonuclear leucocytes or lymphocytes. 
Their origin is probably from pre-existing, like cells. Thev usu- 
ally have a sluggish movement, are slightly phagocytic and 
also ingest fragments or particles of inert substances. These 
cells may be destroyed or they may emigrate from the affected 
area. 

Wandering connective tissue cells are usually present in 
inflamed tissues. These cells do not appear until some time 



INFLA M M ATION. 



153 



after the injury is inflicted because of their slow movement. 
Their source is from tissue spaces, and they are the preexist- 
ing wandering connective tissue cells that occur in practically 
all tissues of the immature animal. They may be phagocytic 
but this property is not usually well developed. They are es- 
pecially active in the process of repair. 

Giant cells, so-called, are of common occurrence in some in- 
flammatory processes especially tuberculosis and actinomycosis. 
It is probable that endothelial cells are the progenitors of 
giant cells. Some investigators have intimated that wandering 
connective tissue cells may produce giant cells. The giant cells 
mav be formed either by a multiplication of nuclei without divi- 












j^^--^^- 



<9"--^ 






Fit 



-C-astritis, hog, induct d by a caustic, showing destruction of gastric 

mucosa. 



sion of the cell body or by a fusion of several independent cells 
(Syncytium). The latter view is the one most accepted at the 
present time. The function of the giant cell has not been 
specifically determined, but those in tubercular lesions fre- 
quently contain many tubercle bacilli indicating that they are 
phagocytic. 

Red blood corpuscles or erythrocytes occur in the inflam- 
matory exudate as a result of intense engorgement of the ves- 
sels. They begin passing through the vessel wall after the 
leucocytic migration. Increased intravascular pressure is the 
principal cause of their escape from the vessel, their passage 
through the vessel wall being entirely passive. 



154 



VETERINARY PATHOLOGY. 



2. Varieties. — Inflammatory exudates m^y be serous, fibrin- 
ous, or hemorrhagic. 

a. A serous exudate continues in the fluid state as long as it 
remains in the tissues or tissue spaces. It is composed almost 
entirely of fluid, having very few cells. This variety of ex- 
udate is characteristic of mild inflammatory conditions. The 
constancy of the fluidity of the serous exudate is the result of 
the action of enzyms that continually convert the albuminous 
substances into soluble compounds as proteoses and peptones. 

b. Inflammatory fibrinous exudate contains two enzyms, one 
of which (leucoprotase) is active in an alkaline medium and 
the other in an acid medium. ''These enzyms probably exert 
their greatest activity in a neutral medium, slight changes in 
reaction increasing digestion by the one, and suspending di- 




Fig. 94. — Acute Pleurisy, 

a. Engorged vessels. 



b. Exudate. 



gestion by the other." In suppuration the acid digesting enzym 
probably disappears (Barker). A fibrinous exudate is one 
that coagulates within the tissues or tissue spaces. The coagu- 
lation of the exudate is identical with the coagulation of blood 
and is probably due to the liberation of fibrin forming enzyms 
from disintegrated leucocytes. Fibrinous exudate is the variety 
observed in inflammation resulting from severe irritation. The 
exudate usually contains many cells and a large amount of 
proteids. 

c. Hemorrhagic exudates are those in which the red blood cells 
as well as leucocytes and plasma have passed through the ves- 
sel wall. This exudate coagulates the same as the fibrinous 



IXFLAMMATIOX. 155 

exudate. Intense irritants are usually the causative agents of 
hemorrhagic inflammation. Croupous pneumonia is character- 
ized by a hemorrhagic exudate. 

A so-called purulent exudate has been described but pus is 
not purel}^ exudative for some of its constituents are not de- 
rived from the blood. Pus is composed of altered leucocytes, 
tissue shreds, and usually bacteria, suspended in a fluid, liquor- 
puris. Liquor puris is blood plasma and dissolved tissue. Pus 
contains no fibrin, the proteid constituents being converted into 
soluble compounds by cellular enzymes and bacterial ferments. 

3. The following are probably the determining factors of the 
quality and quantity of inflammatory exudate. 

a. Cause of inflammation : — Generally speaking a mild irritant 
or injury produces a serous inflammation, and an intense ir- 
ritant produces fibrinous inflammation. Mechanical injuries,, 
when there are no surface abrasions, produce an inflammation 
of a mild degree and the exudate is limited m quantity and is 
usually of a serous nature. Such injuries, however, usually 
produce abrasions which favor the invasion of micro organisms. 
Thermal disturbances of mild degree, produce a serous ex- 
udate, if more severe the exudate is extensive and of a fibrin- 
ous or hemorrhagic character. The use of a thermo-cautery is 
an excellent example of thermal production of inflammation and 
the severity of its use demonstrates the intensity of inflamma- 
tion and the variations of the exudate. An irritating chemical 
substance injected into a tissue produces inflammation char- 
acterized by excessive exudation especially of a serous fluid. 
T'le more irritating the chemical, the greater the quantity of 
exudate and the greater the percentage of proteids. External 
application of chemical irritants produces inflammation char- 
acterized by a serous or by a fibrinous exudate. This latter 
may be observed in the application of blistering agents. In- 
fective inflammation is usually accompanied by a marked exu- 
date from the beginning of the infection. The quantity and 
quality of the exudate varies with the virulency of the organ- 
ism. There are some exceptions hov/ever, e. g., tetanus infec- 
tion causes a very limited exudate regardless of the virulency 
of the tetanus bacillus. In some infections, as malignant 
oedema, the exudate is largely fluid. In suppuration the ex- 
udate is almost entirely leucocytic. 

b. Condition of the animal effected. The exudate is usually 
limited in animals having normal vessels, heart action, and 
blood. In those animals in which the vessels are diseased and 
especially if the endothelium has been injured there is a ten- 



156 



VETERINARY PATHOLOGY. 



dency to excessive exudation. A weak heart is conducive to 
excessive exudation, e. g., inflammatory oedema. Animals pos- 
sessing dilute blood (hydremia) are predisposed to excessive 
fluid exudation. The leucocytic amoeboid movement may be tem- 
porarily suspended, or it may be increased during inflamma- 
tion, resulting in an absence or in an excessive number of 
leucocytes in the exudate. In animals having a clean close 
build the exudate is not so extensive as it is in those animals 
of a loose flabby make-up. 

c. The location and tissue aflfected. Exudation is in direct pro- 
portion to the vascularity and density of the tissue. Inflam- 
mation in compact bony tissue or beneath dense facia, liga- 




Fig. 95. — Acute Meningitis. 

Exudate. b. Engorgred vessels. 



tnents or tendons is accompanied by a limited exudate. In- 
flammation of the cutaneous structure is usually associated 
with excessive exudation, which accumulates in the subcutane- 
ous areolar tissue. Inflammation of serous and mucous mem- 
branes is accompanied with exudation which may in part be 
discharged upon the surface but is usually accumulated in the 
substructures. 

4. Significance of the exudate. — The significance of the exu- 
date has had various interpretations. Virchow considered that 
the irritation producing the inflammation resulted in increased 
cellular activity in the injured area and that the exudate sup- 
plied increased nourishment to the area in which there was 
an excessive metabolism. Others have attributed to the exudate 
the "flushing out" of the injured area thus mechanically carrying 



INFLAMMATION. 157 

away the irritant. The exudate dilutes the irritant, especially 
chemical irritants, thus reducing the activity of the causative 
agent and mitigating the inflammatory process. 

It has been determined that serum possesses some sub- 
stances, as opsonins, antitoxins, bacteriolysins and bactericides, 
that are detrimental to infectious agents either by their bacter- 
icidal action or by chemical union with bacterial products. 
Thus the exudate reduces the irritation of infection by render- 
ing bacteria inactive or by neutralizing their products. Phago- 
cytes are very important factors in the exudate as they ingest 
and destroy infectious micro-organisms. The opsonic index 
championed by Wright of London is based on the above. 




Fig. 96. — Inflammation. Gray Hepatization. 
a. Air cells en.?orged with leucocytes. b. Hyperemia of capillaries. 

In aseptic incised wounds the exudate is of value in cementing 
the incised surfaces together, although new tissue formation is 
retarded by an exudate. The exudate mechanically protects the 
injured surfaces in gaping wounds and possesses bactericidal 
properties for a short time after the injury has been inflicted. 
After the exudate becomes inactive in its protecting properties 
it is a favorable medium for infection and is then probably 
detrimental. Injurious chemic substances may result from the 
aseptic dissolution of an inflammatory exudate. 

Fibrinous exudates may be injurious or beneficial depending 
upon the location and the changes taking place in the exu- 
date. The fibrinous exudate in croupous pneumonia is injuri- 
ous because it coagulates in the alveoli of the lung thus pre- 
venting the respiratorv function of that area. The fibrinous 



158 



VETERINARY PATHOLOGY. 



exudate in serous cavities is beneficial, especially in localized 
inflammation, because it limits or circumscribes the inflamma- 
tory irritant or process by coagulating thus producing adhe- 
sions of the two serous membranes. Many horses upon which 
paracentesis abdominis or paracentesis thoracis is performed 
might succumb to generalized peritonitis or pleurisy if the 
inflammatory process established at the point of the puncture 
was not circumscribed by adhesions the result of organization 




Fig. 97. — Fibrinous Pleurisy, showing an extensive exudate upon surface, 



of fibrinous exudate. The immediate efifect of a fibrinous exu- 
date in a serous cavity is beneficial but the adhesions are fre- 
quently permanent thus interfering with the normal function- 
ing of the part affected. The fibrinous exudate is also benefi- 
cial in croupous enteritis because of the protection of the dis- 
eased mucosa from mechanical injuries by food stuffs. It is 
on the other hand injurious in croupous enteritis for the exu- 
date is a favorable nidus for bacteria and they may produce 
substances that are irritating to the injured mucosa. The 
coagulated exudate may also hinder intestinal secretion. The 



INFLAMMATION. 159 

fibrinous exudate of diphtheritic inflammation is very injurious 
because of its coagulation and pressure upon the tissues. 

Chemotaxis. — It has been determined by experiment that 
chemic substances exert a definite influence upon motile cells. 
There is always a leucocytic migration into capillary glass tubes 
previously charged with turpentine or croton oil and then in«^ert- 
ed into living animal tissues. The same migration is obse.-ved 
when the capillary tubes are charged with bacteria or their 
products. Negative results are obtained when the tubes are 
charged with quinine or chloroform. This attraction of leuco- 
cytes tow^ard chemic substances is positive chemotaxis. The 
repulsion of leucocytes from chemic substances is negative chem- 
otaxis. The term "Chemotaxis" unmodified includes positive 
and negative. Leucocytic migration into an inflammatory area 
is a result of chemic influence or chemotaxis. 

Phagocytosis. — This is the incorporation and destruction of 
pathogenic bacteria and other foreign substances by phagocytes. 
Phagocytes are cells having the power of ingesting and destroy- 
ing microorganisms and other foreign particles. Polymorpho- 
nuclear leucocytes having neutrophile granules are the most ac- 
tive cells concerned in phagocytosis. Endothelial cells and wan- 
dering connective tissue cells may be under some conditions 
phagocytic. The phagocytic property of cells is variable depending 
upon the virulency of the micro-organisms or strength of the 
chemic substance and upon the resistance of the phagocyte. Bac- 
teria are enveloped by protoplasmic extensions from the cell 
body imtil they are entirely included in the aggressive phago- 
cyte. After the enveloping process there may be observed diges- 
tion vacuoles surrounding the bacteria. The included bacteria 
are destroyed by ferments produced by the phagocyte. It is an 
intracellular digestion. The length of time necessary for the 
phagocyte to destroy the bacteria is variable. The bacterial 
destruction may be instantaneous or the bacteria may possess 
sufficient vitality to destroy the phagocyte. There is consider- 
able evidence that infection is frequently generalized in the ani- 
mal body by leucocytes that have enveloped bacteria and wan- 
dered to another portion of the body. The included bacteria 
destroy the leucocyte and, thus liberated, establish a new cen- 
ter of infection. 

Phagocytosis is a very important factor in inflammation. 
No doubt many localized inflammatory conditions are aborted 
and the intensity of the attack of other infective inflamma- 
tory conditions reduced by the process of phagocytosis. There 
is a peculiar variation of phagocytosis occasionally observed, 



160 



VETERINARY PATHOLOGY. 



e. g., leucocytes becoming phagocytic toward other leucocytes. 
Fixed tissue cells may under some conditions become phago- 
cytic towards leucocytes; this perhaps is for the purpose of 
obtaining nutrition for the fixed tissue cells. 

The Signs of Inflammation. — Inflammation may be recognized 
in exposed tissues by the so-called ''Cardinal signs:" redness, 
swelling, increased temperature, pain and impaired function. 
These signs are usually perceptible in the early stages of acute 
inflammation, but they may not be evident throughout the entire 
process. Mild, chronic inflammation may not be accompanied by 
any of the above signs. These signs are very variable in either 
acute or chronic inflamm_aticn of internal organs. 




Fig. 9S. — Acute Myositis. 

a. Leucocytis exudate. Muscle fibres disintegrated and vessels engorged. 



Redness (Rubor) is a constant sign in the early stages of 
acute inflammation. It is the result of an excessive amount of 
blood in the vessels of the affected area. 

• Swelling (Tumor) is characteristic of acute inflammation. 
It is the result of the accumulation and retention of the inflam- 
matory exudate pKis the increased amount of blood in the part. 
The extent of the swelling is in a direct ratio to the density of 
the tissue. Thus the swelling resulting from subperiosteal in- 
flammation mav not be detected because of its limited extent. 
On the other hand, the swelline succeeding: inflammation of 
loose areolar tissue may be very extensive, as in cellulitis. The 
swelling resulting from inflammation is usually firm, dense and 
quite resistant in contradistinction to swelling resulting from 



INFLAMMATION. 161 

oedema, e. g., the tumefaction accompanying tendonitis is dense, 
while the swelling accompanying "stocking" is soft and doughy. 

The temperature (Calor) of tissue affected with active in- 
flammation is invariably increased. This is the result of the 
excessive cellular action in the inflamed area and the increased 
amount of blood flowing into the part. 

Pain (Dolor) is a common symptom of inflammation. This 
may be the result of pressure upon nerve endings bv the accu- 
mulated exudate. However, oedema is accompanied by an ex- 
cessive accumulation of fluid in the tissues, and oedematous 
tissues are not hypersensitive. It seems more probable that in- 
flammatory pain is the result of the injurious action of the 
irritant or soluble products of the exudate upon the sensory 
nerve endings. The inflammatory pain is often referred to some 
other part of the body, e. g., in pleurisy the pain frequently 
appears abdominal. 

Impnired function (Functio laeso) is a constant feature ob- 
served in inflammation. In the beginning of the process the 
function of the affected tissues (especiallv secretory) is in ex- 
cess of the normal, but this is succeeded in the later stages by 
depression of the function. The increased function is a result 
of increased nourishment, increased stimulation, and probably 
increased pressure is also a factor ; the depressed or diminished 
function is the result of the injurious action of katabolic prod- 
ucts, produced by excessive cellular action, and of the irritant 
producing the inflammatory process. Thus, in the beginning 
of acute nephritis there is an excessive amount of fluid (urine) 
excreted, this is succeeded by diminution or complete suppres- 
sion of the excretion (urine). 

Effects upon the Tissue Involved. — As a result of 
the inflammatory process the tissues involved may un- 
dergo various changes. These changes may be degenerative, 
necrotic, regenerative or proliferative in character. Degenera- 
tion usualh^ precedes regeneration, but the two conditions may 
be independent of each other ; thus in ulceration, degeneration 
and necrosis may alone be evident, and in the formation of a 
tubercle of tuberculosis proliferation is the principal process. 
Both conditions may exist at the same time in different parts 
of an affected area, degeneration taking place in the center of 
the diseased area and regeneration or proliferation in the peri- 
phery. Inflammation not accompanied by either degeneration 
or regeneration is rare. The injuries or irritants establishing 
inflammation may and frequently do produce death of some of 
the tissue cells ; necrotic tissue is sufficiently irritating to pro- 



162 



VETERINARY PATHOLOGY. 



duce inflammation, and necrotic areas are usually surrounded 
by an inflammatory zone. Inflammation is confined to the 
reactive process of the injured cells and should not be confused 
with the death of the cells or necrosis. 

Degeneration and regeneration are distinctly opposite pro- 
cesses. The former is destructive, resulting in impairment and 
death, while the latter is constructive, resulting in overgrowth 
and proliferation. Degeneration is caused by insufficient food, 
inhibition of irritating products, or excessive and frequently 
perverted functional activity. Regeneration occurs when there 
is an adequate supply of nutrition, and depends upon the rever- 




Fig. 99.- 



a. Alveolus. 



-Chronic Pneumonia. 

c. Wandering leucocytes. 



Fibrous proliferation. 



sion of the cells to the embryonic type or stimulation of the 
reproductive properties of the cells, the latter usually at the 
expense of the normal functional activity. Both processes af¥ect 
the cellular elements of the tissues, primarily and actively, and 
the intercellular substances secondarily and passively. Some 
exceptions will be mentioned later. The leucocytes and wander- 
ing cells may also undergo changes similar to those which the 
fixed tissue cells are subject. In general, degeneration character- 
izes acute inflammation and regeneration characterizes chronic 
inflammation. The importance of either of the above processes 
depends upon their extent The general consideration of the two 
processes has been combined for the sake of comparisoii ; but 
they will now be considered separately. 

Degeneration. — Practically all degenerations, to which tis- 



INFLAMMATION. 163 

sues in general are subject, are common in inflamed tissues. 
The following are the principal ones that have been described. 

1. Parenchymatous degeneration (cloudy swelling), is the most 
common type in acute inflammatory tissues. It is indeed rare 
to examine sections of tissue affected with acute inflammation 
and not find this degeneration. The presence of parenchymatous 
degeneration is an additional factor frequently resorted to in diff- 
erential diagnosis of inflammation. This type of degeneration 
occurs in all tissues, but more especially in glandular structures. 

2. Fatty degeneration does not occur as frequently as paren- 
chymatous degeneration. Like parenchymatous degeneration, 
it occurs in tissues affected with acute inflammation. It in- 
variably occurs in combination with parenchymatous degenera- 
tion and is usually a sequel of the latter. The presence of fatty 
degeneration in inflammatory tissue may cause confusion in 
microscopic diagnosis, especially if the degeneration is exten- 
sive. The degeneration is common in epithelium (glandular), 
muscular tissue and connective tissue. 

3. Mucoid degeneration is quite common is inflamed tissues. 
It is characteristic of catarrhal inflammation. This degenera- 
tion affects the intercellular substance as well as the cells. 
Mucus is bactericidal, therefore it is protectant and beneficial, 
unless produced in sufficient quantity to induce mechanical in- 
jury. Epithelium and connective tissue are most frequently 
affected by this degeneration. 

4. Serous degeneration, or more properly infiltration, is char- 
acteristic of tissues affected with inflammatory oedema or other 
inflammations in which there is excessive serous exudation. 
This con.dition results from the passage into the cells of extra- 
cellular serous fluid. The infiltrated fluid mechanically inter- 
feres with the activity of the cell. It occurs most frequently 
in muscular and connective tissue and occasionally in epi- 
thelium. 

5. Hyaline degeneration is of common occurrence in tissues 
affected with chronic inflammation. It is the conversion of the 
tissue into a clear, waxy substance. It is common in the mus- 
cular tissue of blood vessels in chronic inflammatory foci as 
well as in fibrous tissue resulting from proliferative inflamma- 
tion. 

6. Amyloid degeneration has been observed in chronic inflam- 
matory tissues (Adami), although this is not a common sequel 
of inflammation. 

An intercellular degeneration specifically affecting the ce- 
ment substances between the myocardial cells has frequently 



164 VETERINARY PATHOLOGY. 

been observed in myocarditis. This causes a separation of the 
heart muscle cells, i. e., fragmentation, which seriously inter- 
feres w^ith their function. The striations of muscle cells fre- 
quently disappear as a result of inflammation. 

Necrosis (local death). — All degenerations produce impair- 
ment of function and frequently end in necrosis of the affected 
cells. Destruction of tissue is a common result of inflammation 
because of the various degenerations that accompany the in- 
flammatory process. Suppuration is a type of inflammation and 
is a liquifying necrosis. Necrosis of inflammatory tissue often 
occurs independently of suppuration, though both conditions 
result from the same cause. Destroyed tissue constitutes a fac- 
tor in the future changes that occur in the affected tissue. 
Superficial necrotic tissue is usually cast ofif. Ulceration is the 
condition resulting from a continuous and sometimes a pro- 
gressive cellular necrosis. An ulcer is a denuded surface result- 
ing from continuous and sometimes a progressive cellular 
necrosis. 

Subsurface necrotic tissue may be disintegrated or dissolved, 
and pass out of the affected area in the exudate or be carried 
out by phagocytes ; necrotic tissue may become surrounded and 
permeated by large numbers of leucocytes which liberate dis- 
solving ferments, thus forming an abscess ; this liquefied necro- 
tic mass may become inspissated, a condition termed caseation ; 
the necrotic tissue may become impregnated with calcium salts, 
denominated calcification ; finally, the necrotic tissue may be- 
come dissolved and encapsulated, thus forming a cyst. 

Regeneration. — This process usually begins when degenera- 
tion ceases, although it may be evident from the first. Cells 
concerned in regeneration undergo a reversionary change, be- 
coming similar to embryonic cells. Reproduction is an active, 
vital property of embryonic cells, and this is also the principal 
function of regenerating cells. The appearance of a tissue con- 
taining an exudate with the succeeding degeneration has been 
previously discussed. A concise comprehension of such tissue 
is essential to a clear conception of the appearance of regenera- 
tion in an inflammatory zone. Whether degenerated cells are 
capable of regeneration depends upon the kind of cells and the 
extent of the injury to them. Regeneration of tissues impaired 
or destroyed by acute inflammation consists in the enlargement 
and proliferation of the contiguous uninjured cells. The exu- 
date is usually diminished in quantity at this stage. Prolifera- 
tion in tissues afifected with chronic inflammation is, in reality, 
a fibrous hyperplasia. Cirrhosis of any structure is usually the 



INFLAMMATION. 



165 



result of chronic inflammation. The lowest types of tissues, 
i. e., those passive in function, are most easily and most fre- 
quently regenerated, e. g., connective tissue. Surface epithe- 
lium is frequently regenerated — muscular and nervous tissues 









^ 

























t 



^\ 



^^. 















,\ f, KKf^' «% ":"." ! *"^^^^*'° ^ •- ^ - '^ '- 






^. ^\^ \ \«-**>, 



.-it,-- 100. — Chronic Hepatitis, showing intralobural fibrous formation, whicli results 

in hypertrophic cirrhosis. 

are rarely regenerated. The age of the individual is an im- 
portant factor in the regeneration of injured tissues. Tissues 
in young animals regenerate more readily than like tissues in 
old animals. 

The origin or source of the cells that regenerate connective 



166 VETERINARY PATHOLOGY. 

tissue is still a disputed point. It is certain that fixed and wan- 
dering connective tissue cells are capable of this function. 
Endothelial cells are a type of fixed connective tissue cells which 
are active in regeneration of connective tissue. Mononuclear 
leucocytes as well as lymphocytes may be capable of producing 
connective tissue. The regenerating connective tissue cells 
(fibroblasts) are either oval or spindle shaped, the.: latter pre- 
dominating, especially during the active regeneration period. 

Endothelial cells are active in the production :.of new vessels. 
Inflammatory tissue is usually more vascular than normal tissue. 
In the vascularization of an inflanimatory area the endothelial 
cells produce long protoplasmic projections. Several of these 
projections of different adjacent cells may fuse/ thus forming an 
anastomotic channel, or a single projection may separate in a 
longitudinal direction, thus producing an extension of the old 
channel. As the protoplasmic projections become larger and 
longer there is an activity in the cell nucleus indicative of 
mitosis, and cell division soon follows. This process of proto- 
plasmic projections and mitosis continues as long-, as the in- 
flammatory process is active. The irregular blood channels 
(capillaries) so formed become surrounded by a layer of invol- 
untary muscle tissues and yellow elastic tissue as a result of 
extension of muscle fibres and connective tissue cells from the 
adjacent vessel, the whole structure being surrounded by a 
loosely arranged layer of white fibrous connective tissue. Thus 
the capillary becomes an arteriole. These cells that are active 
in vascularization are designated angioblasts. They are the 
progeny of endothelium. 

Inflammatory injuries to surface epithelium, as epidermis or 
mucous membrane, are usually repaired by multiplication of the 
ceMs bordering the injury. 

Irregular masses of nucleated protoplasm have been observed 
in myositis and may represent regenerating muscle cells. 

Kinds or Types or Inflammation. — It is difficult to classify 
inflammation because of the numerous variable factors that com- 
pose it. The following classification is based upon etiology, 
exudate, tissue involved, and time or severity of attack. 

Etiology. — Etiologically, inflammation may be classified as 
simple and infective. 

1. Simple inflammation is noninfective and results from me- 
chanic, thermic, electric or chemic interference. 

Fractures, sprains, bruises and surgical-procedure wounds 
are types of mechanic inflammation. 

As types of thermic inflammation, burns and frozen tissues 



INFLAMMATION. 167 

may be mentioned. Local inflammatory disturbances resulting 
from lightning or contact with electric currents are types of 
electrically established inflammation. The following may be 
mentioned as chemic inflammations ; formalin dermatitis, ar- 
senical enteritis, chlorine pneumonitis, turpentine nephritis, and 
those induced by the bites of poisonous reptiles, scorpions, bees, 
wasps and ants ; also those caused by the products of bacteria 
and animal parasites. The inflammatory processes established 
by mechanical interference may and usually do become infected 
either by external contamination or bv the deposition of infec- 
tious agents from the blood or lymph. 

2. Infective Inflammation is of more frequent occurrence 
than non-infective. It is the kind of inflammation that concerns 
the practitioner, veterinary inspector and sanitarian because of its 
tendency to become generalized in the infected animal, and is 
frequently transmissible to other animals. All tissues are sus- 
ceptible to infective inflammation except hair, wool, feathers, 
and the insensitive, nonvascular portions of the teeth, hoofs, 
claws and horns. Infective inflammation may be either non- 
suppurative or suppurative. 

(a) Nonsuppurative infective inflammation is typified in mal- 
ignant oedema, blackleg, localized anthrax and the earlier stages 
of tuberculosis ani actinomycosis, and is characterized by the 
general phenomena of inflammation previously discussed. In- 
fective inflammation may be nonsuppurative in the earlier stages 
and in the later stages be complicated by typical suppuration, 
as in tuberculosis. IMore rarely nonsuppurative inflammation 
continues throughout the entire process, as in blackleg. 

(b) Suppurative infective inflammation or suppuration. — 
Suppuration is liquefying necrosis, and may be surface or subsur- 
face, circumscribed or diffuse. The liquefied necrotic tissue pro- 
duced by suppuration is pus. Pus is a fluid, varying from a thin 
watery substance to a thick, sticky, tenacious mass,^~and is usu- 
ally alkaline in reaction. The color of pus is determined by the 
infective agent, and it may be white, lemon yellow, golden yellow, 
greenish yellow, green or black, and is frequently tinted red 
with blood. Pus obtained from horses, donkeys and mules is 
usually w^hite or grayish white ; from cattle, creamy yellow ; 
from sheep, greenish yellow, and from hogs, green or greenish 
yellow. Pus is usuallv odorless, although it may undergo pu- 
trefaction wnth the evolution of ill-smelling gases. Actinomy- 
cotic pus has a nutty odor (Mayo). Pus may have a greasy, 
smooth, stickv or granular feel when rubbed between the fingers, 
depending upon its composition. 



168 



VETERINARY PATHOLOGY. 



Histologically, pus is composed of pns cells, i. e., leucocytes 
(the most of which are necrotic, though some of them may pos- 
sess vitality), shreds of necrotic tissue and tissue cells (the type 
of which depends upon the tissue affected), usually pyobacteria 
in varying numbers (many of them being included in the pus 
cells) and liquor puris (the plasma or fluid portion of the exu- 
date and the fluid resulting from the solvent action of the vari- 
ous ferments). Animal microparasites are found in the pus re- 
sulting from their activity. Practically all of the pus cells are 
derived from polymorphonuclear leucocytes, and are usually the 
neutrophile variety, there being only an occasional mononuclear 
leucocyte. Extensive nuclear fragmentation and parenchyma- 
tous and fatty degeneration of the cell protoplasm are evident in 
most pus cells, indicating that they have undergone necrosis. 
Degeneration or necrosis are also present in the fixed tissues of 
the suppurative areas. The pus found in acute abscesses or dis- 
charging from granulating wounds is usually a creamy fluid, 
yellowish in color. Sanious pus is a reddish fluid resulting from 
an admixture with blood. Ichorous pus is an acrid, corrosive 
fluid that excoriates the tissues it contacts. Muco-pus and bv^ro- 




Fig. 101. — Drawing of a pus smear from a case of strangles, showing the organism 
arranged in chains — the Streptococcus pyogenes equi. 



INFLAMMATION. 169 

pus are mixtures of mucous and pus, and of serum and pus, 
respectively. Putrid pus is a thin, ill-smelling fluid, the result 
of putrefaction. 

Infection is the usual cause of suppuration. The following 
is a brief description of the process. Pyogenic micro-organisms 
gain entrance either by deposition upon or into a wound by 
passing through the tissue or are carried and deposited by the 
blood or lymph, and, finding conditions favorable, develop and 
multiply. In their development, pyobacteria produce chemic 
substances that are sufficiently irritating to establish an active 
hyperemia and also to exert a positive chemotactic influence, 
the latter attracting at first mononuclear leucocytes and later 
causing the migration of neutrophilic polymorphonuclear leuco- 
cytes to the focus of infection. Multiplication of the pyobac- 
teria and leucocytic immigration continue. Phagocytosis be- 
comes evident in leucocytes and some other cells, e. g., endo- 
thelial cells. Liberated ferments, produced by the pyobacteria, 
leucocytes and other cells, cause degeneration, necrosis and, 
finally, solution of the tissue involved. Continued pyobacterial 
multiplication stimulates an increased leucocytic immigration. 
and the tissues are thus densely packed with cells. There is a 
marked accumulation of leucocytes around the suppurative focus 
apparently attempting to circumscribe the affected area. Thus 
the process continues, there being a progressive liquefying cen- 
tral necrosis within and a marginal leucocytic accumulation 
without. The condition is repeated until the resistant influences 
of the animal body destroy the pyobacteria, or until the pyo- 
bacteria have destroyed the involved tissue, or the entire ani- 
mal. (Suppurative osteitis may occur subperiosteal or in the 
osseous tissue proper. Leucocytes invade the lacunae and pro- 
duce solution of the mineral matter, and thus the bone becomes 
porous. If this process continues the bone ultimately liquefies ; 
this is termed caries.) 

Surface suppuration (purulent inflammation) is suppuration 
of a surface tissue. Pas produced in surface suppuration con- 
stitutes a purulent discharge, and a persistent purulent discharge 
is termed pyorrhoea. Inflammation of a mucous membrane ac- 
companied by a purulent discharge is purulent catarrh. In puru- 
lent catarrh the surface epithelium is infiltrated with leucocytes 
frequently to such an extent that the epithelial cells are disin- 
tegrated, become loosened and exfoliate. The surface cells of 
serous membranes and the skin are similarly affected in purulent 
inflammation. In any purulent inflammation there is always 



170 



VETERINARY PATHOLOGY. 



an engorgement of the subsurface vessels and the related areo- 
lar tissue is infiltrated with inflammatory exudate. 

Subsurface suppuration may be circumscribed or diffuse. 
Suppurative centers become circumscribed first by a dense wall 
of leucocytes and later by a fibrous capsule. The capsule is in 
nearly all cases denser on the side next to the more important 
tissue. Fibroblasts that form the circumscribing fibrous capsule 
are probably the wandering connective tissue cells or their 
progeny. The collection of pus in tissues, or lymph spaces, and 
as considered by some in body cavities, constitutes an abscess. 
The circumscribed pus may, by solvent action of its ferments, 




Fi£ 



a. Normal kidney tubule. 



102. — Suppurative Nephritis. 

b. Suppurative focus surrounded by kidney tissue. 



dissolve or erode the limiting structure (cells or capsule), and be 
liberated ; the erosive action being in the direction of the least 
resistance. In this way a surface discharge is effected. The 
channel of exit of the pus may persist and become circumscribed 
by a fibrous wall, thus forming a fistulous tract. If the pus 
cavity is completely evacuated by surgical interference or other- 
Avise, and the cause removed, the surrounding tissue will, by 
proliferation, fill the space previously occupied by the pus. The 
pus in an abscess may be absorbed and the destroyed tissue be 
replaced by regeneration. If the capsule is exceedingly dense 
the contained pus may become caseated and calcified. 

Abscesses may be classified as superficial and deep ; primary 
or metastatic (metastatic abscesses may or may not be embolic), 
simple or multiple, subfascial and intermuscular. A hot abscess 



INFLAMMATION. 171. 

results from rapid, active suppuration, as submaxillary abscesses 
in strangles, while the so-called cold abscess results from a slow 
suppurative process, as in tuberculosis. Accumulations of pus 
in body cavities as the peritoneal, pleural, pericardial, synovial 
and the facial sinuses constitute empyema. A'esicles may be- 
come infiltrated with leucocytes, which become pus cells, and 
thus the vesicle becomes a pustule. 

Diffuse suppuration is not limited by any definite border line. 
It is the result of agencies possessing sufficient strength or 
virulency to continuously and progressively destroy and liquefy 
tissue or it occurs at a time wdien the resistance of the animal 
or its tissues is so greatly diminished that there is inabilit}^ to' 
successfully antagonize the causative agent. Purulent infiltra- 
tion is the permeation of tissues w^ith pus. Phlegmonous in-' 
flammation is the rapid and usually extensive infiltration of 
tissues with leucocytes (pus cells), and occurs most frequently 
in the subcutem and submucosa. 

Exudate. — According to the nature of the exudate inflammation 
tion may be classified as serous, fibrinous, and hemorrhagic. 
The physical properties, chemic and histologic composition of 
inflammatory exudate has been previouslj^ discussed. 

(a) Serous inflammation is characterized by a serous exudate. 
Inflammation of serous membranes and inflammatory disturb- 
ances of other tis-sues than serous membranes, caused by mild 
irritation, may be of this type. Occasionally serous --inflamma- 
tion is the result of intense irritation as in malignant oedema. 
The terms serous inflammation and inflammation of serous 
membranes should not be used interchangeably, because in- 
flammation of serous membranes may be characterized by 
fibrinous or hemorrhagic exudate. A circumscribed accumula- 
tion of inflammator\' serous fluid (exudate) in the deeper lay- 
ers of the epidermis or mucosa constitute a vesicle. Inflam- 
matory oedema, a serous inflammation, is the condition result- 
ing from the diffusion of an excessive amount of inflammatory 
serous exudate into tissues as in cellulitis (inflammation of 
sub-cutem). 

(b) Fibrinous inflammation designates that type of inflammatory 
disturbances in which there is produced a coagulable exudate. 
The exudate mav coa-gulate within the tissues or upon the tis- 
sue surface. Croupous inflammation is the term applied to the 
condition resulting from the coagulation of the exudate upon a 
tissue surface. Diphtheritic inflammation is the condition pro- 
duced bv coagulation of the exudate within the tissue and 
upon its surface. Croupous inflammation and diphtheritic in 



172 



VETERINARY PATHOLOGY. 



flammation are not distinctly separable although the former is 
usually milder than the latter. Typical croupous exudate may 
be detached without serious injury to the surface tissue but 
the diphtheritic exudate cannot be removed without detaching 
or extensively lacerating the surface tissue. Croupous pneu- 
monia and croupous enteritis are examples of croupous inflam- 
mation, the former being the most frequent type of pneumonia 
in horses and the latter occurring occasionally in cattle. Roup 
or avian diphtheria, and diphtheritic stomatitis and enteritis are 
examples of diphtheritic inflammation, the former being com- 
mon in fowls the latter in pigs. Fibrinous exudate may be 
present in inflammation of serous membranes, constituting 
fibrinous pleurisy, peritonitis, etc. 

(c) Hemorrhagic inflammation is significant of the action of 
an extreme irritant. Hemorrhagic exudate coagulates, especially 
upon surfaces, though it may coagulate within a tissue. Inflam- 
mation of tissues in which the blood vessels are of meager struc- 
trure (capillaries), and hence easily permeated or ruptured, is fre- 
quently of this type. Croupous pneumonia is a hemorrhagic in- 
flammation. Nephritis and hepatitis are frequently accom- 
panied by a hemorrhagic exudate. 

(Mucus and pus have been described as inflammatory exu- 
dates by some and as inflammatory products by others.) They 
















.oj 



Fig. 103. — Hemorrhagic Exudate (Red Hepatization.) 



INFLAMMATION. 173' 

are not inflammatory exudates. Inflammation of mucous mem- 
branes in which there is an excessive production of mucus is 
catarrh or catarrhal inflammation. (Suppuration is inflammation 
accompanied by the formation of pus and may be surface or sub- 
surface. Purulent inflammation is surface suppuration.) 

Tissue. — Histologically a gland or organ is composed of 
parenchymatous and interstitial tissue. Parenchymatous tissue 
is the essential or functioning portion of a structure, as hepatic 
cells. Interstitial tissue or stroma is the supporting framework 
of an organ or part as the stroma of a lymph node. The pro- 
cess of inflammation may occur in either the parenchyma or 
stroma. Classifying upon the basis of tissue affected then, there 
are the two forms, namely, parenchymatous and interstitial in- 
flammation. 

(a) Parenchymatous inflammation is usually the result of 
severe, active irritation, the interstitial type results from the 
long, continued action of mild arritants. The two types may be 
present simultaneously in the same structure or they may occur 
independently. 

(b) Interstitial inflammation is often the sequence of paren- 
chymatous, although it may be the initial process. Inflammation 
of the hepatic cells is parenchymatous hepatitis, of the hepatic 
interlobular tissue, interstitial hepatitis, etc. 

Time, Activity and Results of the Process. — It is questionable 
if the length of time an inflammatory process continues should 
constitute a factor in its classification. By common usage, inflam- 
mation would be classified according to the time basis, as acute 
and chronic. Formerly this classification was based upon the 
time element alone, but the duration of inflammation is so vari- 
able that it is now recognized as an insignificant factor. The 
activitv and results of the process are the basic essentials relied 
upon in differentiating acute and chronic inflammation. 

(a) Acute inflammation is characterized by a sudden onset, by 
a vigorous action and by production of retrogressive changes in 
or destruction to the tissue affected. 

(b) Chronic inflammation is characterized usually by an 
insiduous onset, by a mild action, and by resutling in prolifera- 
tion of tissue. The proliferated tissue may induce retrogressive 
changes, as atrophy, but this is only an indirect result of the pro- 
cess. 

Either acute or chronic inflammation may occur throughout 
the entire reaction or they may both prevail at the same time in 
different parts of the same structure. The causative agents may 
become less active as the process continues, thus acute inflam- 



174 VETERINARY PATHOLOGY. 

mation is often succeeded by chronic inflammation. Injuries of 
tendons are usually accompanied by acute inflammation, but 
this usually subsides early and is succeeded by chronic inflam- 
mation. Chronic inflammation may be succeeded by acute in- 
flammation provided that the irritating factor be sufficiently in- 
creased or the resistance of the animal diminished. 

Miscellaneous. — a. Catarrhal inflammation is inflammation of a 
mucous membrane, accompanied by an excessive production and 
discharge of mucus. 

b. Purulent inflammation is characterized by the production 
of pus. This term is confined, by some, to surface suppuration. 

c. Ulcerative inflammation is one in which there is erosion 
of surfaces, i. e., the production of ulcers. 

d. Vesicular inflammation is one characterized by the pres- 
ence of vesicles. 

e. Pustular inflammation is one characterized by the pres- 
ence of pustules. 

f. Proliferative inflammation is practically the same as 
chronic inflammation. It signifies the production of new tissue, 

g. Specific inflammation is one resulting from a specific in- 
fection, as glanders. 

Termination.— The tendency of the reaction produced by 
an injury is always favorable, but the reaction may be so sud- 
den and extensive or continued so long that its results may 
be harmful. The termination of inflammation depends upon the 
extent, intensity, and duration of the irritant and the resistance 
of the tissues. Inflammation may terminate in resolution, tissue 
proliferation or dissolution. 

Rcso'Iution embraces the processes of repair and these may 
be summarized as follows : 

a. Removal of the cause. 

b. Re-establishment of circulation. This may be accom- 
plished in a few hours or perhaps not for several days depend- 
ing upon the extent of the injury and the kind of tissue injured. 

c. Restoration of vessels to their normal condition. The 
length of time required for restoration and the completeness of 
the process depends upon the severity of the injury and the re- 
establishment of the circulation. 

d. Removal of the inflammatory exudate. The time re- 
quired to remove the exudate depends upon its nature. Serous 
exudates are usually removed by resorption, i. e., by the lymph 
channels. Fibrinous and hemorrhagic exudates are usually dis- 
solved and absorbed, or they may be carried away by phagocy- 



INFLAMMATION. 175 

tes. Exudates may in part l^e consumed as nutrition by local 
cells. 

e. Disposal of necrotic tissue. Necrotic tissue is disposed of 
by sloughing, absorption, phagocytosis, or sequestration. Small 
areas of necrotic tissue are usually promptly absorbed or dis- 
posed of by phagocytic action. Considerable time is usually re- 
quired in disposing of large areas or masses of necrotic tissue, 
unless it is superficially located and separates from the surround- 
ing tissue and sloughs. Subsurface necrotic tissue mav be gradu- 
ally liquefied and absorbed, discharged through a fistulous tract 
(submaxillary abscess of Strangles), collected and carried out 
by phagocytes, encapsulated, or sequestrated, and remain per- 
manently in the tissue. Encapsulated necrotic tissue may be- 
come infiltrated with calcium, salts. 

f. Regeneration of degenerated tissue and replacement of 
necrotic tissue. The regeneration of degenerated tissue consists 
in replacing the injured or destroyed cell protoplasm by normal 
protoplasm. If only a few cells are destroyed the adjacent cells 
reproduce and thus renewal is usually rapid. Connectiye tissue 
cells and surface epithelium are easily and efficiently regenerated, 
but cardiac muscle, ganglionic nerye and cartilage cells are 
rarely perfecthr regenerated. Large areas of necrotic tissue are 
usually substituted by fibrous tissue. This proliferated tissue is 
termed granulation tissue in the beginning and cicatricial tissue 
after it has become dense and more or less contracted. Granu- 
lation tissue consists of capillary loops surrounded by masses 
of cells. These cells are largely fibroblasts and produce fibro- 
connectiye tissue. After the fibro-connectiye tissue has been 
formed it contracts, thus becoming cicatricial tissue. Cicatriza- 
tion is of yalue in closing gaping wounds, but is injurious when 
it occurs in internal organs as the liyer, because the pressure 
produces atrophy and obstructs circulation. The capsule sur- 
rounding pus cavities, after the purulent fluid has been evacuated, 
becomes a granulating membrane which soon fills the gap with 
fibrous connective tissue. Exuberant granulation results from 
excessive multiplication of cells, undue extension of capillary 
loops, and failure of contraction of the fibrous tissue. 

Tissue Proliferation. — The tissue proliferated in inflammatory 
resolution takes the place of tissues that pre-existed and had be- 
come necrotic, while that occurring in inflammation resulting 
from long continued mild irritation is not a substitution but an 
addition to the tissue already existing. In this latter phase 
tissue proliferation may begin in a very short time after the in- 
flammation is established or it may not appear for two. three, 



176 VETERINARY PATHOLOGY. 

or several days. Fibro-connective tissue is invariably the pro- 
duct of tissue proliferation. Fibro-connective tissue prolifera- 
tion is closely associated with chronic inflammation, in fact it is 
almost inseparable from it. The proliferated tissue appears first 
in the frame-work of the tissue involved and may later extend 
into the parenchymatous tissue. If the proliferated tissue is 
excessive it may, by pressure, produce atrophy of the parenchy- 
matous tissue. Cicatrization of the proliferated tissue causes an 
irregular lobulation and constriction of the involved organ, as 
in cirrhosis of the kidney. Strictures of hollow organs are pro- 
duced in the same way. Adhesions of serous membranes are 
produced by fibrous tissue formed during inflammation. 

Dissolution or destruction is a result of intense irritation. 
Necrosis of tissue is frequently a sequence of inflammation. A 
single cell or only a few cells may be destroyed or large areas 
of tissue may undergo necrosis. Ulceration results from con- 
stant cellular necrosis. Circulation may be obstructed by an 
inflammatory exudate and cause necrosis in large masses of 
tissue. It may terminate fatally, in partial recovery, or in reso- 
lution, depending upon the importance of the tissue involved in 
the affected animal. 

Conclusion. — Inflammation is the reaction of a living tissue 
to an irritant. 

Inflammation is a complex process, the result of many fac- 
tors. 

It is not always a result of infection. 

It is an adaptive, reparative and protective process. 

It mav produce sufficient reaction to cause destruction of 
the portion involved and occasionally of the entire organism. 



CHAPTER VII. 

PROGRESSIVE TISSUE CHANGES. 

REGENERATION. 

DEFINITION. 

EXTENT — Depends upon age and tissue involved. 
Blood. 

Connective tissue. 
Fibrous. 
White. 
Yellow. 
Cartilage — Rarely regenerated perfectly. 
Bone. 
Epithelium. 

Surface — Complete and perfect. 
Glandular — Irregular and incomplete. 
Muscle — Perfect regeneration rare. 
Nerve — Cells do not regenerate, Hhres do. 

Regeneration is the process by means of which destroyed 
tissues are replaced. Tissue destruction is the result of necro- 
sis, primarily, and inflammation and degeneration, secondarily. 
Regeneration is accomplished by multiplication of pre-existing 
adjacent cells or by invasion and multiplication of wandering 
connective tissue cells. The proliferating cells assume the charac- 
teristics of embryonal cells, that is, their reproductive property 
is over-developed and their other vital functions depressed. The 
power of regeneration of a tissue is inversely proportional to its 
specialization. Regeneration of the tissues of the less complex 
animals is more nearly perfect than that of the tissues of highly 
organized animals ; thus invertebrates regenerate entire organs 
or parts. Spallanzani cut off the legs and tail of a salamander 
and observed in the course of three months six crops of these 
members. In the entire three months 687 perfect bones were re- 
produced and the regeneration was perfect regardless of the 
point of amputation* The tissues of young growing animals are 
more easily regenerated than those of mature animals. Single 
cells or small areas of tissue are more perfectly regenerated than 
large areas. In some cases destroyed tissues are not regenerated 
but are replaced by fibrous tissue. The functions of some de- 
stroyed tissues and organs may be performed by other struc- 
tures. Thus, if the tibia of a dog is destroyed, the fibula in- 
creases in size and assumes its function. Destruction of one 
kidney is succeeded by a compensatory hypertrophy of the other 

177 



178 



VETERINARY PATHOLOGY 



kidney. The law of specificity, i. e., cells beget like cells, is 
the same in regeneration and in physiologic processes. Regen- 
eration is the outcome of the unhindered multiplication of cells. 

Blood is continually regenerated during the natural life of an 
animal. The normal maintenance of blood is a physiologic pro- 
cess, but regeneration of blood or some of its constituents may, 
under certain conditions, be abnormal, as in leukemia. Leuco- 
cytes are produced in lymphoid tissue of the lymph nodes, spleen 
and bone marrow, and it is possible that they may multiply in 
the tissue spaces. Erythrocytes probably have their origin in the 
red marrow of bones in adult animals. The red blood corpuscles 
are nucleated in the beginning but the nucleus vanishes by so- 
lution or extrusion before the cells reach the general circulation 
except in case of severe hemorrhage or other conditions in 
which there has been rapid, extensive loss or destruction of 
blood. 

Blood vessels are usually the first tissue regenerated in the 
repair of wounds. Blood vessels are formed in the embryo by 
canalization of large mesodermal cells, many of which fuse, thus 
forming continuous canals that later become blood vessels. This 




Fig. 104. — Vascular Regreneration, showing vascular buds. 



type of vascular formation is not common in repair of injured 
vessels or regeneration of destroyed vessels. The usual manner 
of vascular regeneration is by the growth and development of 
endothelial buds from adjacent vessels. These buds are solid, 
conical processes which extend outward from the capillarv en- 
dothelium. The buds or processes increase in size and become 
hollow at their base, the cavity being thus continuous with the 
Hmicn of the pre-existing vessel. As the buds increase in size 



PROGRESSIVE TISSUE CHANGES. 



179 



.there is an increase in the number of cells composing them. 
Union or fusion of buds or processes from different vessels re- 
sults in anastomosis or inosculation. These processes are thus 
the forerunners of capillaries and by a dilatation and an increase 
in the thickness of their walls due to formation of fibrous and 
muscular tissue, arteries and veins are formed. The new vessels 
produced in the repair of an injury are invariabty in excess of 
the normal vascular requirements of the part. The excess ves- 
sels in an injured area are obliterated by cicatrization. 

Connective tissue is usually completely regenerated. Con- 
nective tissue is regenerated from pre-existing connective tissue 
cells, wandering cells and endothelial cells. 

Mucoid connective tissue is not normally found in the adult 
animal except in a modified form in the vitreous chamber of the 
eye. Mucoid tissue is not regenerated, although it is possible 
that other types of regenerated connective tissue are mucoid in 
the beginning. 

Fibrous connective tissue is rapidly and completely regen- 
erated. White fibrous connective tissue is frequently substi- 
tuted for other tissues. The fibres in regenerated fibrous con- 




Fig. 105. — Fibrous Reg^eneraticn. 



nective tissue have the same origin as those in normal fibrous 
tissue. Regeneration of white fibrous tissue may be studied in 
the union of the ends of a tendon after tenotomy. The space 
between the ends of the tendon is filled with blood and lymph 
which escaped from the severed vessels. The pre-existing con- 
nective tissue cells bordering- the wound in the tendon, tosfether 
with wandering cells, begin proliferating within forty-eight 
hours, their progeny being fibroblasts. The fibroblasts produce 
a tangled mass of fibrous connective tissue, and at the same time 
there is vascularization of the extravasate which occupies the 
space between the severed ends of the tendon. After the ends 



180 VETEiRINARY PATHOLOGY. 

of the tendon are firmly united by the mass of newly formed 
fibrous tissue the extravasate and the fibres, excepting those ex- 
tending in a longitudinal direction, are absorbed. Finally the 
repair is so complete that the defect is not visible to the unaided 
eye and is difficult to detect microscopically. Scars are bands, 
sheets or masses of white fibrous tissue and indicate imperfect 
regeneration, the fibrous tissue in scars being largely a substitu- 
tion tissue. 

Yellozv elastic tissue is not as perfectly regenerated as white 
fibrous tissue. White fibrous tissue usually is substituted for 
yellow elastic tissue when the latter has been destroyed. 

Regeneration of cartilage is very imperfect probably because 
of its irregular supply of nourishment. Destroyed cartilage is 
usually replaced by fibrous tissue. In some instances injuries 
to cartilage are succeeded by excessive cartilaginous prolifera- 
tion. A case was observed in which the arytenoid cartilage was 
severed in an operation to relieve roaring; six months later there 
had developed at the point of operation a cartilaginous mass as 
large as a goose ^gg. Perfect regeneration of cartilage does 
occur, although it is rare. Regenerating cartilage cells are de- 
rived from the inner portion of the perichondrium. Fibrous 
tissue formation usually precedes the regeneration of cartilage, 
alth/^"i^h it may be formed from the beginning. 

Osseous tissue is usually perfectly regenerated . The cells 
that produce osseous tissue are called osteoblasts. Osteoblasts 
are usually derived from the osteogenetic layer of the perios- 
teum, although they may have their origin from undifferentiated 
connective tissue cells. The formation of osseous tissue is usu- 
ally preceded by mucoid, fibrous or cartilaginous tissue. The 
various stages of osseous regeneration are very similar to those 
of normal bone formation. Osseous regeneration may be illus- 
trated by the union of a fracture as follows : Blood and lymph 
vessels are ruptured when the fracture is produced. Blood and 
lymph escapes into the surrounding tissues and the interstice 
between the two ends of the fractured bone. The injury pro- 
duces necrosis and establishes inflammation. Vascularization of 
the injured area initiates the process, after which there is solu- 
tion of the extravasate, exudate and necrotic tissue. Osteo- 
blasts accompany the newly formed vessels and produce irregu- 
lar masses of fibrous tissue which later calcify. The calcareous 
tissue is infiltrated with osteoclasts derived from the blood which 
dissolve out regular canals in the regeneration of long bones, 
and irregular cavities in the regeneration of flat or irregular 
bones. Osteoblasts appear in the canals and cavities, formed 



PROGRESSIVE TISSUE CHANGES. 181 

by the osteoclasts, and produce fibrous lamellae which are later 
calcified. This process continues until the canals or cavities are 
filled with lamellae excepting a small central cavity which con- 
tains blood vessels, thus Haversian systems are frequently com- 
pletely regenerated. Excess of osseous tissue formed over and 
around bones at the line of fracture (provisional callous), is 
usually later reabsorbed. 

Adipose tissue is not a typical primary tissue. It is derived 
from the undifferentiated connective tissue cells by the conver- 
sion of their protoplasm into fat. Adipose tissue is consumed 
when the food supply is deficient, and the cells become typical 
connective tissue cells or are destroyed. Adipose tissue is also 
formed when the food supply exceeds the demand as a result of 
production and accumulation of fat in the connective tissue cells. 

Dentine is not replaced except in some of the lower animals. 

Epithelium of surfaces is constantly destroyed and regen- 
erated. The outgrowth and shedding of the superficial epi- 
dermal cells is a physiologic process. Epithelization of small 
abrasions of the epidermis and mucous membranes is rapid and 
complete, the regenerating cells having their origin from the 
epithelium bordering the injury. If the denuded surface is large 
regeneration ma}- proceed from the cells of the sweat glands 
of the skin, or mucous glands of mucous membranes as well as 
the epithelium bordering the injury. 

Squamous epithelium is more completely regenerated than 
columnar. Constant destruction of columnar cells mav cause 
the production of short columnar cells and finally squamous 
cells. This, however, is rare, as the law of specificity is practi- 
cally without exception. Glandular epithelium is not regenerated 
as perfectly as surface epithelium (excepting the sweat glands, 
oil glands, mucous glands, gastric glands, Brunner's glands, 
crypts of Lieberkiihn and uterine glands). Any of the foregoing 
will regenerate from, small islands of cells either in the duct or 
body of the gland. The epithelium of the mammarv gland in- 
creases in amount during lactation and diminishes when lacta- 
tion ceases. By observation it has been determined that mam- 
mary epithelium regenerates after it has been destroyed bv ab- 
scess formation or other destructive processes, provided newly 
formed fibrous tissue is not substituted. By analogy it might 
be supposed that the destroyed epithelium of salivary glands 
and of the pancreas may be regenerated, but this has not been 
clinically or experimentally demonstrated. The liver is a tubu- 
lar gland and regeneration of a single cell or a few cells is not 



182 VETERINARY PATHOLOGY. 

uncommon, but large areas of liver tissue are probably never 
regenerated, although some pathologists claim that they have 
observed the regeneration of the major portion of a liver lobe 
in the dog, cat and rabbit. Kidney cells, especially of the tubules, 
are constantly regenerated, although the regeneration of an 
entire tubule has never been observed. The testicular and ovar- 
ian tissues are probably never regenerated except m the physio- 
logic maintainance of spermatogenesis and oogenesis. 

Muscular tissue is imperfectly regenerated. Injuries of invol- 
untary muscular tissue are usually repaired by the substitution 
of fibrous tissue which may later be replaced by involuntary mus- 
cular tissue, the latter being derived from the adjacent muscle 
cells. Two or three days after an injury to a voluntary muscle 
fibre, the nuclei near the injury divide and a multinucleated 
protoplasmic mass is formed on the damaged fibre. These pro 
toplasmic masses extend into the substituted fibrous tissue and 
may split longtitudinally into regular fibres but more frequently 
they die and disintegrate. Destroyed heart muscle cells are 
invariably replaced by fibrous tissue. 

Nerve cells are not regenerated, at least in adult animals, 
although their processes, axones and dendrites, are regenerated in 
peripheral nerves. After a nerve fibre is injured the axone 
degenerates to the distal end and to the first or second node of 
Ranvier proximally. A few days after the injury the axone, if 
its continuity has not been destroyed, begins to elongate, ex- 
tending peripherally, in the direction of least resistance, which 
is in the old sheath. If the axone extends in the original sheath 
the tissue deprived of its nerve supply may become perfectly 
innervated. The rate of growth of an axone has been variously 
estimated at from .1 mm. to 1mm. in twenty-four hours. Foot 
lameness in horses that has been completely relieved by meta- 
carpal and metatarsal neurectomies, sometimes reappear, in 
from eighteen months to three years after the operation, thus 
indicating that there has been reinnervation. If the proliferating 
axone does not continue in the original nerve sheath it may 
become entangled and coiled up in the scar tissue, of the wound, 
thus producing sensitive scars and amputation neuromata. 



PROGRESSIVE TISSUE CHANGES. 183 

WOUND HEALING. 
DEFINITION. 
CLASSIFICATION. 
Etiology. 

Traumatic. 

Thermic. \ 

C hemic. -• 

Location. 

Surface. 

Subsurface, {Cephalic, cervical, thoracic, etc.) 
Character. 

Incised. 

Punctured. 

Lacerated. 

Contused. 

Stab. 

Gun shot. 

Bites. 
Condition. 

Aseptic. 

Septic. 
HEALING. 

Primary union, (First Intention.) 

Hemorrhage arrested. 

Approximation of zvound margins. 

Adhesion of zvound lips with -exudate. 

Multiplication of related cells. 

Vascularization. 

Epithelization. 
Secondary union, {Second Intention.) 

Hemorrhage arrested. 

Immigration of leucocytes to wound margins. 

Infection. 

Suppuration. 

Granulation. 

Cicatrisation. 

Epithelization. 

The regeneration of the individual tissues has been discussed. 
The simultaneous regeneration of the tissue-complex of an area 
in which there has been previous tissue destruction constitutes 
wound healing. A wound is the result of sudden interruption of 
the continuity of tissue or tissues. Some have restricted the 
term 'wound' to those conditions resulting from traumatisms ; 
others confine it to injuries of soft tissue, and again some main- 
tain that wounds occur only upon a surface. There is no good 
reason for restricting the term, because both thermic and 
chemic influences produce tissue destruction not distinguish- 
able from wounds mechanically inflicted. A fracture is a break 
in the continuity of osseous tissue and is repaired in the same 
way as wounds of soft tissue. Rupture of the liver or spleen is 
characterized by tissue destruction and regeneration, the entire 
process being identical with that in surface wounds. Wounds 
result from sudden and violent action. Thus ulcers or necrotic 



184 VETERINARY PATHOLOGY. 

tubercular centers are not wounds. A bruise may or may not 
be a wound, depending upon the nature of the lesion, i. e^, 
whether or not the interruption of tissue has been affected. 

Wounds may be classified as to cause, location, character, and 
condition. 

1. Etiologically wounds may be traumatic, thermic or 
chemic. 

2. According to location wounds may be, surface or subsur- 
face, abdominal, cervical, thoracic, etc. 

3. As to their character, wounds may be incised, punctured, 
lacerated, contused, stab, shot, or bullet and from bites. 

4. Wounds may be noninfectious and infectious. 

Traumatic wounds usually heal more readily than wounds re- 
sulting from thermic or chemic causes because traumatisms are 
caused by mechanical force only and the destructive influence 
ceases immediately upon removal of the cause ; whereas the in- 
fluence of thermic and especially chemic causes are more lasting 
as their action continues after the wound has been produced. 

Wound healing may be of one of two types, healing by pri- 
mary union (first intention), and healing by granulation (sec- 
ond intention or secondary union). These two modes of heal- 
ing differ only in extent. Other methods of healing have been 
described as immediate union, healing by third intention, and 
healing under a scab. Immediate union, signifies union of parts 
of a cell or the cut ends of fibres, etc., and is now thought to be 
impossible ; healing under a scab and healing by third intention 
are properly discussed under the caption of primary union or 
granuation. 

Healing by Primnrv Union. — This is the most desirable 
method of wound healing and is usually obtained in veterinary 
practice only in surgical wounds and recently inflicted, clean cut 
wounds. This mode of healing is of short duration and is ac- 
companied by little if any infection and limited inflammation. 
Healing by primary union takes place only in clean cut wounds, 
i. e., when the tissues are smoothly and evenly divided and in 
which hemorrhage is limited and easily controlled. After hem- 
orrhage ceases or has been arrested the extravasate coagulates 
thus agglutinating and drawing the wound margins together. 
If the incised surfaces or severed tissues be approximated by 
surgical procedure the coagulated extravasate and exudate as- 
sists in maintaining them in that position. In surface wounds 
.varying quantities of serum and lymph discharge and coagulate 
upon the surface thus forming a scab. The injury producing 
the wound and the extravasate are sufficiently irritating to es- 



PROGRESSIVE TISSUE CHANGES, 



185 



tablish hyperemia and in some cases slight inflammation ac- 
companied by a serous exudation and a leucocytic immigration. 
The hemorrhagic extravasate is gradually disintegrated and re- 
moved by phagocytes and at the same time, there is enlarge- 
ment and extension by multiplication of the marginal tissue 
cells of the wound into the coagulum which serves as a support 
for the regenerating tissue. 

Vascularization -accompanied by fibrous formation initiates 
the process of regeneration in the healing of a wound 
by primary union. Vascularization is usually limited because 
of the small size of the wounds. The newly formed vessels 
are capillaries and supply the regenerating tissue. Fibrous 
tissue is produced in sufficient quantities to replace all tissues 
destroyed. 

Disintegration of the coagulum and regeneration of new tis- 
sue thus proceed until the newly formed tissue has entirely re- 
placed the extravasate. The scab is firmly held upon the wound 




^^^-^^sT^S^^ ^"^ ^'M^ 



Fig. 106. — Wound Healing by first intention, 

a. Fibrinous exudaie wiih pruliteiation of vessels. c. Bottom of wound. 

b. Regeneration of epithelium. d. Leucocytes. 



186 VETERINARY PATHOLOGY. 

by fibrils continuous with the coagulated extravasate and as 
the latter is absorbed the scab gradually becomes loosened and 
finally drops off leaving a shining surface. The regenerated 
tissue formed in the extravasate is embryonic fibrous tissue the 
amount of which depends upon the quantity of coagulum. 
Upon the embryonic tissue thus formed, in surface wounds, 
epithelization is usually rapid and complete. The scar appears 
pale pink and is tender until cicatrization takes place and then 
appears white, dense, firm and hard. Whether the fibrous tis- 
sue produced in wound healing is substituted later by the nor- 
mal tissues of the part involved depends upon the generative 
power of the tissues destroyed. 

To recapitulate, healing by primary union embraces, coagula- 
tion of the hemorrhagic extravasate, agglutination of the wound 
margins, hyperemia, inflammation, vascularization, fibrous form- 
ation, disintegration of the hemorrhagic extravasate and in- 
flammatory exudate, cicatrization, epithelization and substitu- 
tion. 

Healing by granulation. — This is the usual mode of wound 
healing in domestic animals. It differs from the healing by 
primary union in that there is invariably infection and suppur- 
ative inflammation, degeneration and necrosis preceding regen- 
eration. This mode of healing takes place in irregular wounds 
having lacerated margins and in which there is considerable de- 
struction of tissue and extensive hemorrhage and in wounds 
the margins of which are not approximated. The extravasated 
blood may coagulate in the wound, especially in subsurface 
wounds, and also in surface wounds in which the margins are 
approximated and retained by mechanical means, such as su- 
tures, adhesive tape, etc. In lacerated or gaping surface 
wounds, as wire cuts, the coagulum becomes detached and 
drops out leaving the wound margins covered by a thin layer 
of coagulated serum. Within a short time after the injury is 
inflicted there is extensive leucocytic immigration into the tis- 
sues bordering the wound. The infective micro-organisms cause 
destruction and solution of the marginal cells until the tissue re- 
sistance or local immunity checks their activity. Upon the ex- 
posed wound surfaces there appears velvet like projections 
(granulations), which are capillary loops regenerated from ad- 
jacent vessels. 

Between and intermingled with the granulations, regenera- 
tion of connective tissue takes place. Constant exposure of the- 
wound insures continued infection which retards the granula- 
tion more or less, depending upon the extent of tlie infection,. 



PROGRESSIVE TISSUE CHANGES. 



187 



the degree of activity of the micro-organisms and the resistance 
of the tissue. The destroyed tissue in the wound is ultimately 
replaced with granulation tissue and, if the wound is upon t^' e 
surface, epithelization proceeds as in healing l^y primary union. 
The embryonic granulating connective tissue contracts i. e., 




Fig. 107. — Exuberant Granulation, resulting from wire cut. 



cicatrizes about the time that epithelization occurs. Cicatriza- 
tion constricts and obstructs the capillary vessels, that are in 
excess of the normal, thus diminishing the blood supply. If ci- 
catrization does not occur new capillary loops (granulations) 
are rapidly extended producing a fungoid bloody growth, called 
excessive or exuberant granuation (proud flesh). 

The efficient regeneration and substitution of the destroyed 



188 VETERINARY PATHOLOGY. 

tissues in wounds that heal by granulation is possible only in 
very young animals and in tissues not highly organized. 

To recapitulate, healing by second intention embraces sup- 
puration, granulation, cicatrization, epithelization and substi- 
tution. 

In some individuals the formation of fibrous connective tis- 
sue is continuous and there is formed large masses of cicatrical 
tissue known as keloids. Keloids are classified with neoplasms 
by some authors. 



HYPERTROPHY. 

ETIOLOGY. 
Antenatal. 

Unequal pressure. 
Amniotic adhesions. 
Post-natal. 

Increased nutrition. 

Increased function. ' 

Internal secretion. 
Diminished pressure. 
APPEARANCE. 
Macroscopic. 
Microscopic. 
TISSUE AFFECTED. 
EFFECTS. 

Hypertrophy literally means excessive nutrition. By usage 
the term has come to mean, an abnormal increase in the size of 
an organ or part. In a more restricted and definite sense, hy- 
pertrophy is a term applied to that condition resulting from an 
abnormal increase in the size of the essential cells of the part. 
Thus an increase in the size of the liver as a result of an in- 
creased amount of the interstitial tissue or an increase in the 
size of a kidney due to an accumulation of an inflammatory ex- 
udate or oedematous transudate is not an hypertrophy, al- 
though such conditions have been called false or pseudo-hyper- 
trophy. Tumors produce an increase in the size of the struc- 
ture afifected, but this should not be confused with hypertrophy. 
Hyperplasia is a condition resulting from abnormal increase in 
the number of the cells though it is difficult to differentiate 
from hypertrophy. 

Compensatory tiyphrtropiiy is the name applied to that type 
of hypertrophy caused by increased functional activity. Thus 
an increased blood pressure maintained for some time induces 
compensatory hypertrophy of the heart. 

Concentric hypertrophy is a term denoting an hypertrophy of 



PROGRESSIVE TISSUE CHANGES. 189 

the tissues of a hollow organ, accompanied by a diminution in 
the lumen of the hollow organ, e. g., hypertrophy of the heart, 
oesophagus, intestine, or any other hollow organ in which the 
hypertrophied tissues occupy a portion and thus diminish the 
lumen of the organ. 

In some instances hypertrophy represents a normal, physio- 
logic process. The increased size of the pregnant uterus, and 
the enlargement of the mammae during the gestation period are 
examples of physiologic hypertrophy. Increased size of the 
heart and voluntary muscles in horses trained for racing rep- 
resents a physiologic hypertrophy. After the destruction of one 
kidney by disease or the removal of one by operation, the re- 
maining kidney increases in size and ultimatelv performs the 
function of both, this is functional or physiologic hypertrophy 
and also compensatory hypertrophy. In fact practically all hy- 
pertrophies are physiologic, however, the hypertrophied struc- 
tures are abnormal, therefore the condition is pathologic. 

Excessive development of an entire animal i. e., giantism is 
designated by some as general hypertrophy. 

Excessive development of a part as one foot is designated 
local hypertrophy. Local hypertrophy is much more common 
than general hypertropliy. 

Hypertrophy may be inherited, (natural) or acquired. Ac- 
quired hypertroplTy may be antenatal or postnatal. 

Etiology. 

Inhertted hypertrophy. — The cause of inherited hypertrophy 
is unknown except that there is an inherited impulse to grow 
large. This type of hypertrophy is noted in giants. 

Antenatal hypertropity is usuallv the result of unequal pres- 
sure and amniotic adhesions. 

The causative eactors of postnatal itypertrophy are, 1st, in- 
creased nutrition, 2nd, increased function, 3d, a stimulus, prob- 
ably an internal secretion, that causes the afifected tissue to con- 
sume excessive quantities of food. Two or more of these etio- 
logic factors are usually evident in all cases of hypertrophy. 

Increased nutrition. — A long continued, mild arterial hypere- 
mia in a tissue insures increase of the nutritive supply to the 
affected part and such parts usually become hypertrophic. 

Increased function is the prime causative factor of physiologic 
or functional hypertrophy. Increased function is intimately 
associated with increased nutrition, in fact long continued in- 
creased function without increased nutrition is not possible. In 
the production of functional hypertrophy the part must be 



190 VETERINARY PATHOLOGY. 

accustomed to the extra work gradually. An excessive amount, 
of work, assumed at once, by any structure will produce atrophy 
or degeneration. Cardiac hypertrophy is invariably functional 
as it usually is the result of valvular defects. Hypertrophy of 
the involuntary muscle anterior to a stricture is also functional 
as it results from increased muscular action to force the contents- 
of the intestine past the stricture. Voluntary muscular hyper- 
trophy is also functional. 

Some unknown cause is active in the production of certain 
hypertrophic conditions. This unknown cause is probably an 
internal secretion, at least this would appear to be the cause of 
hypertrophy of the mammae and uterus in pregnant animals. 
That certain internal secretions are required to sustain the nor- 
mal balance in the growth of tissues is evident in disease of the 
pituitary body which frequently results in excessive develop- 
ment of certain parts (acromegaly). 

By diminishing the external pressure, experimentally, some 
parts have been noted to become hypertrophic. This is because 
of arterial hyperemia produced by diminished pressure. 

Appearance. 

Macroscopically, h3^pertrophied organs or parts are larger 
and heavier than normal and may be regular or irregular in 
shape. The general appearance of hypertrophied parts other 
than size is not usually sufficiently distinct to differentiate them 
from normal. 

Microscopic. — Renal compensatory hypertrophy is charac- 
terized by increased length and size of the uriniferous tubules. 
Hypertrophy of muscular tissue is characterized by increase in 
the size of muscle cells. In general hypertrophied organs or 
parts contain an excess of parenchymatous tissue. 

Effects. — The effect of hypertrophy varies according to the 
tissue affected. There is usually an increased functional capac- 
ity in an hypertrophied structure. The heart musculature may 
become hypertrophied to such an extent that its force ruptures 
some important blood vessel and causes death. Increased func- 
tion of hypertrophied suprarenal bodies tends to increase 
blood pressure by the production and elimination of large quan- 
tities of adrenaline Avhich causes constriction of arteries and 
cardiac dilation or rupture. 



PROGRESSIVE TISSUE CHANGES. 



191 



HYPERPLASIA. 

DEFINITION. 
VARIETIES. 

Parenchymatous. 

Interstitial, 
ETIOLOGY. 
APPEARANCE. 

Macroscopic. 

Microscopic. 
TISSUE AFFECTED. 
EFFECTS. 

Hyperplasia, according to the derivation of the word, is ex- 
cessive formation. Hyperplasia and hypertrophy are incorrectly 
used interchangeably by some. Hyperplasia should be used to 
designate the condition resulting from an abnormal increased 
size of a part due to an increase in the number of cells of the 
part. Accepting the last definition, hyperplasia mav be due to 
an increased number of parenchymatous cells, or an increased 
number of interstitial cells the two types being called parenchy- 
matous hyperplasia and interstitial hyperplasia respectively. 
Parenchymatous hyperplasia and numerical hypertrophy are 
sometimes used synonymously. Interstitial hyperplasia is prac- 
tically the same as fibrous hyperplasia. 

Parenchymatou.s hyperplasia is not of common occurrence 
It is usually either inherited or congenital. The descended or 
scrotal testicle of single cryptorchids is usually enlarged because 
of an increased amount of parenchyma and hence is an example 
of parenchymatous hyperplasia. 




Fig^. 108. — Hyperplasia Interstitial Testicular Cells. 

a. Interstitial hyperplastic tissue. b. Seminiferous tubules not fully developed. 



192 



VETERINARY PATHOLOGY 



Interstitial hyperplasia is quite common as it is usually evi- 
dent in chronic inflammatory tissues and it is also occasionally 
observed in structures affected w^ith functional fibrosis as is evi- 
dent in the liver of animals afflicted with disturbances of the 
cardiac valves. 

Etiology. 

The cause of parenchymatous hyperplasia is unknown. Inter- 
stitial hyperplasia is produced by the long continued action of 
mild irritants or other substances that produce over stimulation. 

Appearance. 

Macroscopic. — Parenchymatous hyperplastic structures are 
regularly or irregularly enlarged and are heavier than normal. 




Fig. 109. — Pen drawing of an Hyperplastic Ureter, ox, natural size. 



Interstitial hyperplastic parts vary in appearance according 
to the amount of hyperplastic fibrous tissue. The part may vary 
from normal to dense, hard, pale irregularly lobulated masses of 
fibrous tissue. 

M?Vro^<:<9/'?V.— Parenchymatous hyperplastic structures have 
the same appearance microscopically as sections of normal tissue. 

Sections of tissue affected with interstitial hyperplasia con- 
tain an increased quantity of fibrous tissue which may be readily 



PROGRESSIVE TISSUE CHANGES. 



193 



recognized microscopically especially if the section is stained 
with hematoxylin and picro-fuchsin. 

Effects. 

A part affected with parenchymatous hyperplasia will have 
an increased functional capacity. The effects of an increased 
functional capacity of a structure depends upon the part in- 
volved, and may or may not be injurious to the animal in which 
it occurs. 

Interstitial hyperplastic structures have an increased quantity 
of fibrous tissue and usually a diminished amount of parenchy- 
matous tissue and a diminished function. Interstitial hyper- 
plasia of the walls of hollow organs may cause irregularity of 
the lumen (intestine) and hinder passage of the organ's con- 
tents. 

METAPLASIA. 

Metaplasia is the name applied to the conversion of a devel- 
oped or matured tissue into another closely related. Under 
normal conditions a matured tissue has specific cells and a char- 
acteristic structure. The character of a tissue may be changed 
by certain pathologic conditions. Metaplasia should not be con- 



o- 



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<Ly 



^ Z i^^-^ 



>^ * 






fc: 



§« sS' 



%ii © - / „ 



fa ^ 



:r^- - -- ^ ^^^ sot <>■ 






i5> 






.« 



(8 ^ 



«Sng«i 



^»^» 



« 



^. ,^. ^ 







. fl^®*"^ 






35 ^ 



€> 



' r,'^^^ 



Fig. 110. — Fibrous Tissue Ossification. 

a. Fibrous tissue. b. Osteoblasts. 



194 VETERINARY PATHOLOGY. 

fused with degenerative or infective tissue changes which are 
observed in functional or inflammatory fibrous formation. Meta- 
plasia is usually concerned in the conversion of one variety of a 
primary tissue into another variety of the same tissue as fibrous 
tissue into bone and occurs in physiologic processes as well as 
in disease. 

Metaplasia occurs in scars, the conditions consisting of the 
replacement of fibrous tissue by osseous tissue. This type of 
metaplasia is also evident in bone spavin, ringbone, sidebone, as 
well as in scars resulting from fistulous withers, poll evil, etc, 
Metaplastic osseous formation was recently noted in the omen- 
tum of a sheep. The conversion of lymphoid tissue into adi- 
pose tissue is metaplasia. The replacement or substitution oi 
sqnamus epithelium for cubic or columnar epithelium repre- 
sents a type of metaplasia. 

Metaplasia is of little significance except as a pathologic con- 
dition. 



CHAPTER VIII. 
RETROGRESSIVE TISSUE CHANGES. 

DEFINITION. 
ETIOLOGY. 

Variations in nutrition. 

Chemic poisons. 

Chemic reaction of tissue. 

Variations of temperature. 

Variations of function. 
VARIETIES. 

Atrophy. 

Degeneration. 

Iniiltration. 

Pigmentation. 

Physiologic cell growth and function are dependent upon nor- 
mal metabolism. Retrogressive processes are those conditions in 
which normal cell growth and function are diminished or sus- 
pended. Retrogressive tissue changes are caused primarily by 
abnormal cell metabolism or abnormal functioning, and are 
accompanied by structural or chemic alteration of the cell proto- 
plasm or diminution in the size of the cells. 

Metabolic disturbances may be caused by the following: 

Diminished nutritive supply caused by (a) occlusion or di- 
minution of the calibre of nutrient vessels ; (b) insufficient 
supply of food to the animal ; (c) incomplete or lack of digestion 
of the ingested food; (d) failure of absorption of digested food; 
(e) inability of the cells to utilize digested food that has been 
carried to them. Nutrition may be supplied in excess of the 
normal requirements, thus disturbing the metabolic equilibrium. 
Excess nutrients may be stored within the cells or they may be 
converted into energv by oxidation. In the former the stored 
food is a mechanical hindrance to cell action and in the latter 
the cell is overw^orked in converting the food into energy. With- 
holding of nutrient substances from cells produces destructive 
metabolism and ultimately cell death. 

Chemical substances, i. e., poisons exert their action on cells 
by combining with some of the protoplasmic constituents or by 
accelerating, inhibiting or suspending the action of the cell 
enzyms, thus interfering w^ith metabolism. 

Chemic reaction of a tissue influences the action of cell 

195 



196 VETERINARY PATHOLOGY. 

enzyms, and hence is a factor in metabolism and in bringing 
about retrogressive tissue changes. 

Variations in temperaturs. — The various albumens of protop- 
lasm are coagulated at different temperatures. An increase of 3.6° 
F. is sufficient to coagulate one group of albumins and an increase 
of 9° F. is usually fatal because of the coagulation of other impor- 
tant albumin constituents of the cell protoplasm. Fever is invariably 
accompanied by coagulation of some albuminous constituents 
of protoplasm although it is possible that chemic substances as 
well as the high temperature may have some influence in this 
coagulation. Diminished temperature retards metabolic process- 
es and if tissues are exposed for a sufficient time to a low tem- 
perature the protoplasm dies and metabolism ceases. 

Diminished or increased cell functioning are factors in the 
causation of retrogressive changes. Diminished functioning for 
a considerable length of time results in atrophy and if function- 
ing of a specific part is decreased progressively through several 
generations there will be failure of development of that part 
(aplasia). Excessive functioning, to a limited extent, in a 
part supplied with an excess of food, produces hypertrophy. 
Functioning beyond the nutritive supply produces degeneration 
and finally destruction of the cells. 

Retrogressive tissue changes include atrophy, degeneration, 
infiltration and pigmentation. 

ATROPHY. 

DEFINITION. 
DI'FFEREN TIA TION. 
KINDS. 

Physiologic. 
Pathologic. 
ETIOLOGY. 
Physiologic. 
Senility. 
Pathologic. 

Disturbed nutrition. 
Disturbed function. 
Undue pressure. 
APPEARANCE. 
Macroscopic. 
Microscopic. 
TISSUE AFFECTED. 
EFFECTS. 

Atrophy is that condition in which there is a decrease in the 
size of an organ or tissue caused by a decreased size or a dimin- 
ished number of the composing cells. In some instance the 
interstitial tissue increases and replaces the atrophied cells and 
the affected organ does not diminish in size. The term atrophy 



RETROGRESSIVE TISSUE CHANGES. 197 



is usually restricted to a local diminution in size, as, of an organ 
or part, although it has been applied to the condition resulting 
from a general wasting away of all the tissues of the body, i. e., 
emaciation. 

- Atrophy is differentiated from degeneration by the fact that 
the former is purely a diminution in the size of the part, (a result 
of decreased size or diminished number of the cells and without 
any alterations in the cell protoplasm) while the latter consists 
of chemical changes of the cell protoplasm and may result in in- 
creased or diminished size of the cells. Atrophy and degenera- 
tion may occur simultaneously in the same structure, the result- 
ing condition being known as atrophic-degeneration or degenera- 
tive-atrophy. Hypoplasia is an underdevelopment in contradis- 
tinction to atrophy, which is diminution in the size after the 
part has been developed. 

Atrophy may be physiologic or pathologic. 

PHYSIOLOGIC ATROPHY is a term used to designate the normal 
diminution in the size of an organ or part. This occurs in the 
thymus gland which is well developed at the time of birth. Soon 
after this it begins to diminish in size and is practically extinct 
by the time the animal matures. The mammary gland atrophies 
after lactation ceases. Testicles and ovaries atrophy after the 
period of reproduction or sexual activity. Senile atrophy is a 
term employed ta designate all atrophic conditions occurring in 
the tissues of old or aged animals. Senile atrophy is a physio- 
logic process. 

PATHOLOGIC ATROPHY is a term used to designate abnormal 
diminution in the size of an organ or part. Pathologic atrophic 
disturbances involve muscular, glandular and nervous tissue 
although no tissue is exempt. This type of atrophy is of fre- 
quent occurrence, viz., diminution of muscle cells in lameness, 
Sweeney, etc., diminution in the size of the liver in hepatic 
atrophy, renal, cardiac, splenic and gastric atrophy. 

Etiology. — Pathologic atrophy may be the result of either 
disturbed nutrition or disturbed function. 

Disturbed Nutrition. — Atrophic disturbances resulting from 
mal-nutrition are most frequently the result of insufBcient food. 
Cells receiving insufficient food gradually shrink in size, possi- 
bly because of auto-digestion. Insufficient nutritive supply may 
be due to a diminished quantity of blood or an impoverished 
blood. Diminished quantity of blood, i. e., a local anemia, is a 
result of diminishing the calibre or obstructing the supplying 
vessels. 

Thrombic formation, aneurisms, etc., mav cause partial or even 



198 VETERINARY PATHOLOGY. 

complete obstruction of nutritive vessels and thus be a causative 
factor in atrophy. Starvation, or failure, of assimilation of food 
is a cause of atrophy (general). However, in such cases atro- 
phic degeneration of the cells is usually evident by the time the 
body weight has diminished ^/^o of the total weight. Certain 
chemic substances may indirectly be of significance in the pro- 
duction of atrophy, but they influence either the cell nutrition or 
function. 

Excess nutrition may induce metabolic disturbances of suffi- 
cient gravity to cause the cells to become sluggish and more or 
less inactive to such an extent that they will become atrophied. 
However, excess food is a much less frequent cause of atrophy 
than insufficient food. 

Disturbed function. — Diminished or excessive functioning are 
Tcausative factors in producing atrophy, the former being the 
most frequent cause. Tissues deprived of function usually be- 
come more or less atrophied. When an afferent nerve fibre is 
disconnected from its end organ, (the mechanism bv which it 
picks up impressions), it begins to atrophy at once, probably 
because of its failure to function. Muscles not functioning 
atrophy. Thus there is muscular atroph}^ during most cases of 
lameness. Diminished cardiac function resulting from dimin- 
ished blood pressure, is succeeded by atrophy of the heart muscle. 
Glandular structures become atrophied because of disuse. 

Excessive functioning, long continued, causes fatigue and in 
some instances paralysis, the latter usually being succeeded by 
atrophy. Atrophy from excess function is sometimes observed in 
race horses, show animals and is not uncommon in musicians, 
acrobats, trapeze operators, etc. 

Pressure. — Aside from the influence of the vaso-motor mech- 
anism there may be sufficient pressure from tumors, hyperplas- 
tic formations, mechanical contrivances, as harness, etc., to dim- 
inish or obstruct vessels and cause atrophy. Pressure may also 
exert influence other than diminishing the blood supply, for con- 
stant pressure alone causes atrophy, e. g. pressure atrophy of 
osseous tissue. Pressure atrophy, accompanying cirrhosis of 
glandular structures as the liver or kidney, is usually caused bv 
pressure of the newly formed fibrous tissue which partially ob- 
structs the nutrient vessels. However, the compression of the 
parenchymatous cells disturbes their metabolic equilibrium and 
is also a factor of some importance. 

Appearance. Macroscopic. Atrophied organs are usually di- 
minished in size, are irregular or regular in shape, have a dry 
shrunken anemic appearance and are usually pigmented. The 



RETROGRESSIVE TISSUE CHANGES. 199 

parenchymatous tissue is most frequently involved, interstitial 
tissue rarely becoming atrophied. The diminution in size may 
be uniform throughout, the atrophied part thus retaining its nor- 
mal shape, or the diminution may be unequal in different parts, 
thus producing a lobulation of the aft'ected portion. Atrophied 
bone usually maintains its normal external shape, as the process 
is essentially a rarefication in which the Haversian and medul- 
lary canals are increased in size . Pulmonary atrophy may con- 
sist of diminution of the alveolar membranes to such an extent 
that they rupture, thus produciing large cavities. Atrophic mus- 
cular tissue is usually more intensely pigmented than normal 
muscle. The source of the excess pigment in atrophic muscles 
may be from the atrophied muscle cells or it may have its origin 
from the blood. 

Microscopic. — The cell body and nucleus shrink in size in 
simple atrophy without previous alteration in the cell structure. 
In numerical atrophy- the cells first diminish in size and then dis- 
integrate and die. Thus atrophy, disintegration and necrosis are 
evident in numerical atrophy. The appearance of atrophic tis- 
sues vary according to the structures involved. Atrophic kidney 
tissue is characterized by the diminution in the size or in the 
number of the glomerular and tubular cells. The tubules and 
glomeruli may collapse the supplying capillaries becoming oblit- 
erated by pressure of the hyperplastic fibrous tissue. In muscu- 
lar atrophy, the muscle cells diminish in size probably because 
some of the fibrillae disappear. 

Effects. — The eft'ect of atrophy depends upon the structure 
involved the extent of the condition and the age of the animal. 
If the involved structure is not vital and the atrophy is of only 
slight extent and in a young animal, in which the regenerative 
power is good, the part will recover if the cause is removed. 
Extensive atrophy of vital structures in old animals is usually 
fatal or at least predisposes to other conditions that are fatal. 
Again, a part may partially recover after atrophic disturbances. 



200 VETERINARY PATHOLOGY. 

CLOUDY SWELLING. 

DEFINITION. 

OCCURRENCE. 

ETIOLOGY. 

C hemic. 

Bacterial products. 
Phosphorous, Arsenic, etc. 

Thermic. 
APPEARANCE. 

Macroscopic. 

Microscopic. 
TISSUE AFFECTED. 

Epithelium. 

Muscle. 

Nerve. 
EFFECTS. 

Cloudy swelling, albuminous, granular or parenchymatous 
degeneration is a retrograde metamorphosis in which the proto- 
plasm of the cell becomes granular. The granules in cells affected 
with cloudy swelling are albuminous, at any rate they are solu- 
ble in an excess of a 2% solution of acetic acid or a 1% solution 
of potassium hydroxide, and give the typical albumin reaction 
to the xanthoprotein test. Active glandular cells, especially those 
that produce ferments, are normally granular ; but the granules 
in these cells do not respond to the foregoing tests and hence are 
not albuminous. Cells in the earlier stage of fatty degeneration 
are granular but the granules are not dissolved by solution of 
acetic acid or potassium hydroxide, and they are dissolved by 
ether or chloroform and are stained red with Sudan IIL There- 
fore they are fat granules. 

Cloudy swelling probably occurs more frequently than any 
other retrogressive change. It invariably affects parenchymatous 
cells in areas afflicted with acute inflammation and is usually 
associated with infective diseases. 

Etiology. — The causes of cloudy swelling may be divided in- 
to two groups, Chemic and Thermic. 

Chemic substances produce cloudy swelling either by influ- 
encing the action of cell enzyms, thus causing the separation 
(coagulation) of the cell albumins, or by combination with the 
albumins of the cell protoplasm thus forming new compounds 
* (albuminate of mercury, etc.) that are of no value to the cell. 
Excessive quantities of albuminous substances may be assimi- 
lated by the cells, the unused portion becoming coagulated or 
rendered insoluble as it accummulates, thus producing cloudy 
swelling. The chemic substances that produce cloudy swelling 
are usually soluble and are in solution in the blood or lymph 
from which they readily diffuse into the cell body where they 
exert their action. 



RETROGRESSIVE TISSUE CHANGES. 



:oi 



Of the chemic substances capable of producing cloudy swell- 
ing bacterial products are the most important. The diphtheria 
toxin is probably the most active of all bacterial products in the 
production of cloud}- swelling. Other organic substances as leu- 
comains and phenol are capable of producing this degeneration 
as well as many inorganic substances as arsenic, mercury, phos- 
phorous and the mineral acids. 

Thermic disturbances, especially high temperature/ is prob- 
abK' a cause of cloudy swelling. Halliburton has demonstrated 
that certain high temperatures produce turbidity or granular 
degeneration of cells. From experimental evidence it is appar- 
ent that different groups of the albumins of the cell protoplasm 
are separated (coagulated) at dift'erent temperatures. The high- 
er the temperature the more fixed the coagula and the more 
difficult they are of solution. From the present known facts, 
although the chemistry is not determined, it is evident that high 










Fig-. 111. — Cloudy Swelling, showing granular degeneration of kidney cells. 



202 VETERINARY PATHOLOGY. 

temperature is at least a predisposing if not an exciting cause 
of cloudy swelling. 

Appearance. — Macroscopic. — An organ or part alfected with 
cloudy swelling, has a parboiled appearance, it is lusterless and 
lighter in color, softer in consistency, and is slightly enlarged. 

Microscopic. — An organ or part affected with cloudy swelling 
appear cloudy, because of the presence of many small albuminous 
granules, and the cells are slightly enlarged, hence the name 
cloudy swelling. The increased size of the cell results from co- 
agulation, the coagula occupying more space than the non-coag- 
ulated protoplasm. If the tissues of an organ are examined with 
the high power microscope the cell may appear slightly swollen 
and its limiting membrane quite distinct ; it may be considerably 
swollen and have an indistinct membrane ; or, finally, it may have 
ruptured and the space it previously occupied may contain a mass 
of granular debris. The protoplasm of the cell body may con- 
tain small, irregular granules, the nucleus may be almost normal, 
slightly degenerated, or it may even be entirely disintegrated. 

Tissues Affected. — Epithelium, muscular, nervous, and con- 
nective tissue are affected with cloudy swelling, the frequency 
being in the order mentioned. Cells of excretory organs are 
especially affected because of their eliminative function. 

Effects. — The effects of cloudy swelling depend upon the 
structure involved, the extent of the involvment, and the age of 
the affected animal. Affected muscular tissue has a diminished 
contractile power. Renal tubules may be occluded because of 
the swollen tubular cells and the affected cells may also have 
a diminished functional capacity. The function of any structure 
is decreased and in extreme cases inhibited by cloudy swelling 
of its component cells. 

Cloudy swelling is usually a repairable process, providing the 
cause is removed before the cells are destroyed. 



RETROGRESSIVE TISSUE CHANGES. 203 



FATTY CHANGES. 

PHYSIOLOGIC (Fattv I ufilf ration). 
DEFINITION. 
ETIOLOGY. 

Excess food. ■' 

Insufficient exercise. 

Heredity. 

Influence of disease. 

Unsexing. 

Lactation. 

Venesection. 
APPEARANCE. 

Macroscopic — Greasy, pole color. 

Microscopic — Droplets of fat between cells, 
TISSUE AFFECTED. 

Normal depositions. 

Epithelium, innscle. * 

EFFECTS. 
PATHOLOGIC (Fattv Degeneration). 
DEFINITION. 
ETIOLOGY. 

InsiifUcieut food. 

Inability of cells to utilize food. 

Excessiz'e activitv. 
APPEARANCE. 

Macroscopic — Greasy, pale, light. 

Microscopic— Droplets of fat in cells. 
TISSUE AFFECTED. 

Epithelium. 

}Iuscle. 

Nerve. 
EFFECTS. 

Adipose tissue is not a specific tissue, but represents a modi- 
fied connective tissue. The cells that later become fat cells, are 
originally flat or spindle shaped and usually occur in clusters or 
groups. There are certain locations, called fat depositories,, 
where fat usually occurs. Normally the principal fat depositories 
are located in relation to the kidney capsule, subserosa (parietal, 
visceral and omental peritoneum), subcutem, intermuscular areo- 
lar tissue, and in the orbital fossa. A w^ell fattened animal has 
accumulations of fat in all the fat depositories. In an emaciated 
animal limited quantities of fat occur only around the kidney 
in the omentum, and orbital fossa. 

Normal adipose tissue varies in color and consistency in the 
different animals. In general it is white or yellow and appears 
lobulated when cut across. The consistency depends upon the 
melting point of the fat. 

Olein is the principal kind of fat in the hog, stearin and pal- 
mitin in the ox, and stearin in the sheep. It has been demon- 



204 Veterinary pathology. 

strated, however, by Prof. Hopkins, of the University of Illi- 
nois, that the body fat is the same as the ingested fat. (Hogs 
were fed on cotton seed oil and the presence of the same kind 
of fat was demonstrated in the hog tissue.) It has also been 
found that butter fat in cow's milk is the same as ingested fat. 
Opinions are at variance in reference to the digestion and assim- 
ilation of fat. The fat splitting enzyms convert the fats into 
fatty acids and glycerine. The alkali present in the intestines 
unites with a part of the fatty acid, forming soap, the latter and 
the glycerine pass by osmosis into the intestinal epithelium or 
through the mucous membrane where the glycerine is substituted 
for the alkali, the alkali passing back into the intestinal lumen 
to form more soap (Hammersten). Some of the fat may be so 
finely emulsified that it passes directly into and through the in- 
testinal epithelium, and some of it may be incorporated by leu- 
cocytes, and thus carried from the lumen of the intestine to the 
lacteals (Howell). Fat droplets are present in the circulating 
blood. The exact manner of the production of fat cells in normal 
adipose tissue has not been determined. 

All normal animal tissues contain varying quantities of neu- 
tral fat. As much as 23 per cent of fat has been extracted from 
kidney tissue (Adami). The proportion of neutral fat in the 
same kind of tissue varies in the same animal under different 
conditions and in animals of dififerent species under the same 
conditions. Thus the quantity of fat in the muscular tissue of 
an emaciated animal is less than in an animal in good flesh. The 
muscular tissue of the hog contains more fat than the muscular 
tissue of the ox, sheep, horse or dog. In fact the presence of fat 
droplets betwen the muscle cells is a distinguishing characteris- 
tic of porcine muscular tissue. There is no definite limit to the 
quantity of fat normally contained in the tissues of any animal. 

Certain abnormal fatty changes occurring in the various tis- 
sues have been described as fatty infiltration and fatty degen- 
'Cration. These changes, although originally thought to be en- 
tirely distinct, are closely related and may represent dififerent 
Stages of the same process. These fatty changes may be dis- 
cussed as physiologic fatty changes (fatty infiltration), and path- 
ologic fatty changes (fatty degeneration), although there is no 
good reason for the division of the subject other than to recog- 
nize the previous classification and prevent undue confusion. 



RETROGRESSIVE TISSUE CHANGES. 205 

Physiologic Fatty Changes. 

(Fatty Infiltration.) 

Physiologic fatty changes is a condition in which there is an 
excessive accumulation of fat, but the function of the affected 
part is not materially changed. 

Etiology. Excess Food. — House dogs and cats and many family 
horses are usually fed to excess, resulting in the deposition of exces- 
sive quantities of fat in practically all tissues, thus producing general 
obesity. The "Strassburg goose" is force-fed with dough balls 
in excessive quantities until excessive obesity is produced, the 
liver especially becoming the seat of marked fatty accumulations. 
In fact all prime "butcher stuff" is affected with physiologic fatty 
changes or dietary obesity. 

Insufficient Exercise. — Animals kept in tie stalls or in close 
quarters have a tendency to become excessively fat, especially if 
they are fed a full ration, because there is diminished oxidation 
on account of lack of exercise and the bulk of the consumed food 
is stored as fat. 

Venesection. — Frequent bleeding diminishes the percentage of 
red blood corpuscles and thus indn-ectly diminished oxidation 
and favors fat accumulation. 

Disease. — Some diseases appear to influence the physiologic 
deposition of fat. The early stages of tuberculosis in cattle and 
hogs and distomatosis in sheep is accompanied by physiologic 
fatty deposition. During convalescence from some diseases there 
is an increased deposition of fat. 

Lactation. — The early period of lactation is accompanied by 
fatty accumulation especially in the liver. (Possibly the liver 
may act as a distributing center of fat.) The fatty accumulation 
in the liver is evident regardless of any variations in the composi- 
tion of food stuff. 

Heredity. — Some animals, especially hogs, except the Tamworths 
and Yorkshires, appear to have an inherent tendency to become 
excessively fat. 

Castration. — Removal of the genital glands favors fat accumula- 
tion in the tissues. Castrated dogs and cats, especially if cas- 
trated when mature, become obese. 

In general the exciting causes of physiologic fatty changes 
are excess of food or diminished oxidation, heredity being a pre- 
disposing factor. 



206 



VETERINARY PATHOLOGY. 



Appearance. — Macroscopic. — Tissues affected with fatty infil- 
tration are greasy or oily, more friable than normal, and paler in 
color, the color being uniform throughout or mottled. The quan- 
tity of blood in the fat varies, there being more, in general, in 
the fat of young animals. Muscular tissue in which there is a 
fatty accumulation contains areas or strata of fat and strata of 
muscular tissue. Tiie dej^osition of fat may be so extensive in 
muscular tissue of hogs that there is little evidence of muscle. 
Subserous accumulations of fat may be localized, giving the ap- 
pearance of masses of fat, or it may be accumulated dift'usely 
as thick layers of fat. In dogs and cats the excess fat is usually 
deposited around the kidneys. 

Microscopic. — In the early stages of physiologic fatty changes, 
small droplets of fat are observed between and within the cells. 
The intracellular fat gradually increases and assumes the space 
within the cell, the nucleus being crowded to the margin of the 
cell and may ultimately disappear. 




Fig. 112. — Fatty Infiltration, liver, hog, showing- infiltration of globules from 
periphery of lobule toward its center. 



Tissue Affected. — All tissues are subject to fatty accumula- 
tions, excepting the normal depositories, the liver being most 
prone to the affection. 

Effects. — The influence of physiologic fatty changes is de- 
pendent upon the extent of the condition and the duration of 



RETROGRESSIVE TISSUE CHANGES. 207 

the process. If the nuclei of the cells are not injured and the 
process is discontinued the infiltrated fat is disposed of and the 
part recovers. If non-regenerative cells, such as heart muscle, 
are destroyed, they will not be regenerated, even though the 
fat is reabsorbed. The destroyed heart muscle cells may be 
replaced with fibrous tissue. 

Pathologic Fatty Changes. 

(Fatty Degeneration.) 

Pathologic fatty change, or fatty degeneration, is a condition 
in which the protoplasm of the affected cells diminishes because 
of an increase of the intracellular fat. Fat or some of its cleav- 
age constituents is probably constantly present in A^arying quan- 
tities in all active cells. 

Pathologic fatty changes are of frequent occurrence, being 
associated with diseases of malnutrition, and occurring in acute 
febrile diseases and many of the infective diseases, ft is espe- 
cially evident in chronic phosphorous poisoning and some other 
chemically induced diseases. 

Pathologic fatty change is differentiated from cloudy swelling 
as follows : The droplets of fat are soluble in ether and chloro- 
form and are notdissolved with dilute acetic acid or potassium 
hydroxide ; while the granules in cloudy swelling are insoluble in 
ether and chloroform, but are soluble in dilute acetic acid or po- 
tassium hydroxide. Again the fat droplets are stained red by 
Sudan III, while the granules of cloudy sw^elling are not. 
Fatty degeneration is difficult to differentiate from fatty infil- 
tration, and in some instances it is impossible to differentiate 
them ; in fact, future investigation may confirm the identity of 
the two processes. In the early stages the fat droplets are usu- 
ally intracellular in fatty degeneration, and intercellular in fatty 
infiltration. 

Etiology. — In general, fatty degeneration is the result of the 
disturbance of cell metabolism. The production of energy, be- 
ing intimately associated with the metabolism of fat, becomes 
a factor in the causation of fatty degeneration. Specifically, 
disturbed nutrition is the principal cause of fatty degeneration. 
Disturbed nutrition mav be the result of, 1st, variation in the 
composition of the blood, 2nd, diminished quantitv of blood. 3rd, 
diminished oxygen supply, and 4th, changed environments of the 
cells. Insufficient supply of cell nutriment is the principal in- 



208 VETERINARY PATHOLOGY. 

fluence resulting from circulatory disturbances or altered com- 
position of blood. Diminished oxygen supply results in incom- 
plete oxidation of the available intracellular fat which is then 
accumulated within the cell. Changed environments include the 
variation of the chemic reaction of a tissue, the tissue tempera- 
ture, amount of fluid, etc. Disturbance of the environments in- 
fluences the cell metabolism and may cause the union of cleav- 
age products of fat that exist within the cell, or the infiltration 
and intracellular accumulation of fat may be favored. Changed 
environments may also render the cells unable to utilize the food 
brought to them. 

The causes of cloudy swelling are also etiological factors in 
the production of fatty degeneration, in fact, fatty degeneration 
is frequently associated with cloudy swelling and the fatty de- 
generation is the result of disturbed metabolism. Disturbed 
metabolism is produced by insufficient or improper food, dimin- 
ished supply of oxygen, or inability of the cells to utilize the 
food or oxygen supplied, the inability of utilization being a re- 
sult of the damaging influence of chemic or thermic variation 
of the environments of the cells. 

Appearance. — Uacroscopic. — A tissue affected v^^ith fatty de- 
generation varies in appearance according to the extent of the 
process. In general, affected tissues are paler in color (change 
in color is frequently in patches which appear yellowish), lighter 
in weight (in extreme case, liver tissue affected with fatty de- 
generation, floats in water), greasy or oily in appearance, (a 
knife blade that had been used in sectioning a fatty tissue is 
usually smeared with drops of oil or fat), and usually swollen 
or enlarged in the early stages, succeeded by diminution in size 
as the fat is resorbed. Tissues affected with fatty degeneration 
are less elastic, and more friable. 

Microscopic. — In the very early stages the cells contain small 
granules that are differentiated from the granules of cloudy 
swelling only by the chemic test referred to above or by special 
stains, as Sudan III. As the degeneration progresses, the minute 
fat droplets coalesce, forming drops sufficiently large to be rec- 
ognized microscopically, as small, clear spots or holes in the 
cell protoplasm in sections of tissue fixed in fluids that are sol- 
vents for fats and as fat drops in fresh tissues. The affected 
cells are swollen to an extent which is proportional to the degree 
of the degeneration. Ultimately the cell membrane ruptures 
and the enclosed fat is liberated, thus producing a condition not 



RETROGRESSIVE TISSUE CHANGES. 



209 



differentiable from fatty infiltration. The nucleus is usually not 
involved in the beginning, but as the degeneration progresses 
in the cytoplasm, the chromatin network disappears and the 
entire nuclear structure finally becomes disintegrated, producing 
the so-called granule cell. The degeneration may be continuous 
throughout a tissue or it may be more or less patchy. The ex- 
tent of involvement of the cells in an affected area is usually 
unequal, some cells being only slightly affected, others contain- 
ing considerable fat, and still others being entirely converted 
into fat. 




Fig. 113. — ^Fatty Degeneration of the Liver, showing the early stage of the process 

around the central vein. 



Tissue Aflfected — Glandular tissue, particularly the liver, 
is probably most prone to become affected with pathologic fatty 
changes, or fatty degeneration. Muscular tissue is quite subject 
to fatty degeneration, especially heart muscle. Epithelium other 
than glandular, nervous and connective tissues, are not exempt 
from this process. Tumors are occasionally observed to be 
affected with pathologic fatty changes. Necrotic tissue fre- 
quently becomes a fatty mass or an entire cadaver may be con- 



210 VETERINARY PATHOLOGY. 

verted into a fatty mass termed adipocere, w^hich is no doubt 
the result of ferments liberated from the dead tissue. 

Effects. — The conversion of the cell protoplasm into fat im- 
pairs the cell function. At least diminished cell action, as well 
as disturbed cell metabolism is evident in cells affected v^ith 
pathologic fatty change. In cells slightly affected, the droplets 
are either oxidized or are extruded from the cell (absorbed when 
the cause is removed). Cells more extensively affected may be 
destroyed, leaving a meshwork of vessels and fibrous tissue. 
The area may later be filled with the new parenchymatous cells 
arising from the surrounding less affected zones, and, like those 
destroyed, it may persist as a mass of fibrous tissue, i. e., a scar. 
If regeneration occurs there must be an adequate blood supply. 

The degenerated cells may become caseated as a result of 
the conversion of the fatty material into a cheese like mass. 
The usual cause of caseation of fatty debris is diminished or 
obstructed blood supply resulting in gradual absorption of the 
fluids, saponification of the fats and in some instances the forma- 
tion of cholesterin. Caseated material derived from the fatty 
debris may later be liquified or calcified. 



AMYLOID CHANGES. ' 

DEFINITION. 

ETIOLOGY. 

APPEARANCE. 

Macroscopic. 

Microscopic. 
TISSUE AFFECTED— Siiheiidothelium. 
EFFECTS. 

Som.e masses may be found in the acini of the prostate gland, 
especially in old dogs and aged himians, that respond to the iodine 
test and are considered by some authorities as amyloid bodies. 
Physiologic amyloid formations have not been observed other 
than in the prostate gland and they probably have a pathologic 
origin. Thus a physiologic prototype of amyloid formation is 
unknown. 

Amyloid substance (amylin) is an albuminoid, insoluble in 
water, alcohol, ether, chloroform, xylol, dilute acids or alkalies 
and is not acted upon by pepsin. When tissue containing amy- 
loid substances is immersed in Lugol's solution the amyloid 
areas assume a mahogany brown color and the normal tissue is 
stained a yellowish brown. (To make this test wash the affected 
tissue thoroughly until all blood has been removed, apply a lib- 



RETROGRESSIVE TISSUE CHANGES. 211 

eral quantity of Lugol's solution for one or two minutes, wash 
the excess of the reagent oft* and the above color reaction will 
be observed). The test is equally applicable to macroscopic and 
microscopic sections. If the sections, macroscopic or micro- 
scopic, are immersed in dilute sulphuric acid, after the application 
of Lugol's solution, the amyloid area will assume a blue color, 
the normal tissue a brown color. The analine dves usually stain 
amyloid substances some shade of red. 

The source of amylin is not definitely known. It may be 
derived from the blood or from tissue cells. The formation of 
amylin may depend upon variations in the percentage of some 
chemic substance in the blood or tissue juices. 

Amyloid formation is not common in the domestic animals. 
Occasionally a dog is observed that is aft'ected with amyloid ac- 
cumulations in the prostate gland. One case has been observed 
in a hog in which the liver was aft"ected, and, excepting this, the 
carcass showed evidence of no other lesions. 

Etiology. — The cause of amyloid change is not known, al- 
though it has been assumed by some pathologists to be associ- 
ated with chronic suppurative conditions, as, tuberculosis, and 
other chronic debilitating diseases, as carcinomatosis. The 
tissues from several animals affected with chronic suppurative 
processes, as fistulous withers, poll evil, quittor, tuberculosis, 
glanders, caseous-iymphadenitis, as well as tissue from animals 
affected with tumors have been examined, but amyloid changes 
have not been found. Increased or diminished quantity of some 
of the salts of the blood may be found to be an etiologic factor 
in amyloid changes. 

Appearance. — Macroscopic. — Aft'ected tissues or organs are 
larger, paler, and firmer than normal. The amyloid areas are 
homogeneous and translucent in appearance. The entire organ 
or tissue appears homogeneous when the amylaceous material 
is diffuse. 

Microscopic. — Amyloid substance is deposited in the frame- 
work beneath the endothelial cells lining the blood vessels. It 
appears as an annular homogeneous m.ass encircling the vessel. 
The amyloid substance may accumulate to such an extent that 
the vessel is obstructed. After the capillaries have been gorged 
beyond their resistance they rupture, thus allowing the amyloid 
substance to permeate the interstitial spaces where it appears 
microscopically as irregular homogeneous masses. 

Tissue Affected. — The blood-vascular subendothelial con- 
nective tissue is the principal location of amyloid formation, 
although it may occur in lymph vessels and even the perimysium 



212 VETERINARY PATHOLOGY. 

and endomysium may be affected as well as the stroma of the 
mucous membranes. The liver, spleen, and kidney are the 
most frequent locations of the process, probably because of the 
large number of capillaries in those organs. 




Fig-. 114. — Amyloid Denegeration, tiver. 

a. Liver cells. b. Amyloid material. 

Effects. — The condition is so rare that it is not possible to 
generalize upon the effects of the process. The amylaceous ma- 
terial is insoluble in the body fluids and it is quite probable that 
if a part becomes affected, it remains so permanently. 



HYALINE CHANGES. 

DEFINITION. 

ETIOLOGY. 

APPEARANCE. 

Macroscopic. 

Microscopic. 
TISSUE AFFECTED. 

Vessels, Muscles. 
EFFECTS. 

This is a pathologic condition characterized by the conversion 
of the cell substance into a homogeneous material called hyaline. 
In the phenomena accompanying the physiologic changes of the 
corpus luteum of pregnancy, a hyaline substance is produced. 
The physiologic formation of hyalin, aside from that produced 
in the corpus luteum of pregnancy, has not been recorded. 

The formation of hyalin is quite common in the muscular 



RETROGRESSIVE TISSUE CHANGES. 



213 



portion of the blood vessels of tissues affected with chronic in- 
flammation and in the blood vessels of sarcomata. It has also 
been observed in voluntary and heart muscle in certain diseased 
processes. 

Hyalin, an albuminous substance very similar to amylin, does 
not respond to the iodine test, and is not acted upon by alcohol, 
ether, chloroform, acids, ammonia, or water. Acid stains, as 
eosin and acid fuchsin, have an affinity for hyalin and stain it 
quite intensely. 

Etiology. — The specific cause of hyaline formation is not 
definitely known. Certain predisposing factors, however, are of 
interest. Wells found that lactic acid injected into voluntary 
muscle was succeeded by hyaline formation, and it may be as- 
sumed that the cause of hyaline changes in voluntary muscle is 
excess of sarcolatic acid. Some diseased processes, as chronic 
inflammation, tuberculosis, and sarcomatosis are accompanied 
by conditions that tavor hyaline formation. 




Fig. 115. — Hyaline Dcnegration, Vessels. 
a. Hvaline ai'ound arteries in maxilla of colt. 



Appearance. — Macroscopic. — Rarely does this condition be- 
come sufficiently marked to be recognized with the unaided 
eye. The hyaline substance appears as a translucent, homogen- 
eous, firm mass, intermingled with the normal tissue. 

Microscopic. — The hyaline substance appears as glassy areas, 
and the adjacent tissue frequently becomes less distinct. Except 
for the affinitv of hvaline substances for acid stains and its fail- 



214 vp:terinary pathology. 

ure to react to iodine it is difficult to differentiate from amyloid 
change. 

Tissues Affected.- — Muscular tissue, involuntary muscle, 
especially of the blood vessels, voluntary muscle and heart mus- 
cle are subject to hyaline. changes. Connective tissue is less fre- 
quently involved and epithelium rarely, if ever. 

Effects. — When hyaline has been formed in small quanti- 
ties and the cause is removed the hyaline substance is resorbed 
and the affected cells repaired. If the production of hyalin has 
replaced the protoplasm of large cell masses, especially of mus- 
cular cells, the area v^ill probably not be repaired with muscular 
tissue, though it may be with fibrous tissue, provided the cause 
is removed. 



MUCOID CHANGES. 
Physiologic. 

DEFINITION. 

ETIOLOGY — Physiologic, pathologic. 

APPEARANCE. 

Macroscopic. 

Microscopic. 
TISSUE AFFECTED — Connective, epithelium. 
EFFECTS. 

The transformation of cell protoplasm into mucus is evident 
in the physiologic production of mucus in the surface epithelium 
of mucous membranes as well as in mucous glands. The physi- 
ologic conversion of protoplasm into mucus is the result of in- 
tracellular enzyms, or at least depends upon protoplasmic activ- 
ity. As the mucus is produced the cell becomes enlarged and 
ultimately ruptures, discharging the mucus. The miicus may be 
formed only in the distal end of the cell or it may entirely re- 
place the protoplasm of the cell. In the former the remaining 
protoplasm of the cell regenerates the portion destroyed. In the 
latter the adjacent cell multiplies, thus filling the gap. 

Mucus is a viscid, glairy stringy nitrogenous fluid. The 
principal ingredient of mucus is mucin, a glucoproteid, although 
there may also be present pseudomucins. Mucin imbibes water, 
thus becoming swollen, and from this swollen mass there is pre- 
cipitated a stringy material bv addition of alcohol or dilute acetic 
acid. Pseudomucin forms a gelatinous mass when dissolved 
in water, but by the addition of alcohol to this gelatinous mass 
a stringv precipitate is formed which is redissolved in excess of 
water, differing in this respect from mucin. 



RETROGRESSIVE TISSUE CHANGES. 215 

Pathologic. 

Pathologic mucoid formation affects cells and intercellular 
substance. Cellular pathologic mucoid change is identical to 
normal mucus formation except that it is in abnormal locations 
or is in excess in those locations in which mucus is normally 
produced. Intercellular mucoid formation is a condition result- 
ing from the conversion of intercellular substances — fibres, 
matrix of cartilage and bone — into mucus. Pathologic mucoid 
changes occur rather frequently. It is evident in catarrhal in- 
flammation, in cyst formations and as a retrogressive process in 
many tumors. 

Etiology. — The cause of pathologic mucoid changes is not 
known. Excessive cellular mucoid formation accompanies mild 
inflammatory disturbances of mucous membranes — so called 
catarrh. The increased production of mucus in catarrhal inflam- 
mation may be the expression resulting from the exaggerated 
function of the mucous membrane induced by the excessive 
quantity of blood supplied. 

Intercellular mucus formation may result from improper 
nutrition or injurious influences induced by chemic substances. 
It has long been thought, although it has never been proven, 
that some product is evolved when the thyroid gland is dis- 
eased that causes a mucus degeneration of all fibrous tissue in 
the body (myxoedema). Some sarcomata and carcinomata are 
affected with mucoid changes, probably the result of chemic sub- 
stances elaborated by the tumor cells. 

Appearance. — Macroscopic. — ^Mucus of pathologic origin is not 
differentiable from physiologic mucus. In pathologic conditions 
accompanied by mucus formation the mucus is frequently mixed 
with other substances, as blood, pus and food stuff. Thus the 
m.ixture assumes various appearances. A discharge composed 
of mucus and pus (muco-purulent) is common in practically all 
catarrhal inflammation, being the characteristic discharge of 
catarrhal pneumonia and is the usual discharge from the respira- 
tory tract and conjunctiva, in dogs affected wath distemper, in 
horses afflicted with ''stock yard fever," etc. 

The appearance of a tissue affected with pathologic mucus 
changes, regardless of whether the cells or intercellular sub- 
stance is involved, depends upon the quantity of mucus pro- 
duced. If there is a limited quantity of mucus and it is equally 
distributed throughout, the affected tissue will appear swollen 
and soft. If more extensive and diffuse the affected tissue will 
be soft, spongy, and slimy. If the entire structure has practically 
been converted into a mass of mucus, it will appear as a slimy, 



216 



VETERINARY PATHOLOGY. 



Stringy, pulpy substance from which varying quantities of mucus 
may be expressed. 

The mucoid changes may affect circiimscribed local areas that 
appear moist and soft, spongy, or even cystic in contradistinction 
to the surrounding normal tissue. 

Microscopic. — Mucus appears as a stringy substance containing 
varying quantities of detritus. Fixing agents coagulate mucin 
in which case it appears as a more or less homogeneous mass 
containing many fibrillae or threads of coagulated material. 



1 




•~ 


t. 




1 










J"' 


,-;( 

^ 


X 






y 


x' 


4St 


" 


' — J ' ^- __ 




^ ' -^ * ' ■" 


'^-""^ 


im- """ """"-- 


-^^^""^'^ 


ir^^'CT----^ '~ 






Q.--""'Z^--'SZ' 


?^'' ^ ^ 




— — l^ 


c ■ ■ -- 


■■^^ 






;- - 






-l" 








■4 



Fig. 116. — Mucoid Degeneration. 

a. Fibrous tissue. c. Mucoid cells. 

b. Mucous substance. 



Microscopic appearance of a tissue affected with pathologic 
mucoid changes is variable according to the extent of the pro- 
cess but in general the picture observed is the same as that of 
the normal tissue plus the mucus. 

Tissue Affected. — Epithelium and the cells and intercellular 
substance of connective tissue as well as some tumors are sub- 
ject to mucoid changes. 

Effects. — The effects depend upon the extent, duration, and 
regenerative ability of the affected tissue. 



RETROGRESSIVE TISSUE CHANGES. 217 

COLLOID CHANGES. 

DEFINITION. 
ETIOLOGY — Unknown. 
APPEARANCE. 

Macroscopic. 

Microscopic. 
TISSUE AFFECTED. 

Thyroid, prostate, tiiinors. 
EFFECTS, 

The term "Colloid" has rather an indefinite meaning and by 
present day writers is used to indicate a variety of substances. 
"The word colloid is merely morphologically and macroscop- 
ically descriptive of certain products of cell activity or disinte- 
gration, w^hich have nothing in common except the fact that they 
form a thick glue like or gelatinous, often brownish or yellow- 
ish substance" (Wells). One type of colloid substance is a 
physiologic product of the thyroid gland, it is in part a secre- 
tion of the thyroid cells and in part a conversion of those cells 
into colloid material. This product is normally absorbed as it 
is produced though it may accummulate in small quantities in 
the gland acini, especially in aged animals. 

Chemicallv the physiologic thyroid colloid is composed of 
iodo-thyreoglobulin (a compound of globulin and thyroidin). 
Thyroid colloid is glue like in consistency and varies in color 
from brown to yellow. Colloid and mucous are closely related. 
Colloid does not increase in bulk w^hen it is suspended in water, 
neither is it precipitated by alcohol or acetic acid — two tests that 
are usually sufficient for differentiation of mucus and colloid. 
Pseudo-mucin is more difficult to differentiate from colloid. The 
latter, however, contains iodine and the former does not. 

Pathologic colloid changes are conditions resulting from the 
excessive production and retention of collagenous material. The 
disturbance induced by excessive colloid accummulation is usu- 
ally not serious although it may cause fatal termination. This 
condition occurs more frequently in old dogs than in other ani- 
mals. Sheep occasionally show" lesions of this condition, in 
some instances the entire flock becoming affected. Pathologic 
colloid accummulation is a constant lesion in the thyroid gland 
of animals suffering from exophthalmic goitre. Colloid changes 
have been observed in cattle, sheep, horses, mules and one case 
has been recently noted in a calf. 

Etiology. — The specific exciting cause of pathologic colloid 
changes is not known but undue exposure to inclement weather 
is a predisposing cause of considerable moment. Exposure, in 
some instances, appears to become an exciting cause of thyroid 



218 



VETERINARY PATHOLOGY. 



colloid accummulation. A flock of 128 b«althy, yearling sheep 
shipped from south central New Mexico to the Kansas City stock 
yards, were all found to have enlarged thyroid giands at the 
lime of slaughter, which was about 24 hours after their arrival 
at the stock yards. The thyroid glands were found on micro- 
scro'pic examination to be affected with pathologic colloid accum- 
ulation. This occurred in April, the sheep, having been sheared 
just previous to shipment, and the weather having been very 
inclement during the entire time that they were in transit. Other 
entire flocks of sheep that have been unduly exposed have been 
affected in a like manner. 















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Fig. 117. — I hotograph of a tHyruid gland afttcled with Colloid Degeneration, 



Endemic goitre in the human is indicative of an infectious; 
cause though the individual cases in non-affected areas dispels 
the infection theory. 

The absence or diminished quantity of iodine in the food, 
water or air, may be a causative factor in the production of 
goitre and other colloid accummulations in the thyroid glands. 

Appearance. — Macroscopic. — Colloid most frequently oc- 
curs in masses, varying in size from mere microscopic points- 
to bodies as large as a lead pencil rubber or even cyst like bod- 



RETROGRESSIVE TISSUE CEIAXGES. 



219 



ies as large as a black walnut. More rarely the colloid material 
may have infiltrated the tissue spaces and become diffuse. Col- 
loid varies in consistency from a watery to a jelly like mass, is 
usually of a clear amber color, although it may be translucent 
or of a deep mahogany tint. 

An affected tissue contains variable sized areas of hyaline, 
rather firm, amber or mahogany colored masses deposited ir- 
regularly throughout the entire structure. 

Microscopic. — The cells are noted to contain small droplets 
of colloid material which is constantly produced and passed out 
of the cells and accumulated in the acini, tubules, or intercellu- 
lar spaces. Other entire cells are converted into a colloid 




Fig-, lis. — Colloid Degeneration, Thyroid Gland. 
a. Colloid material completely filling- the acini of gland. 



mass. The conversion of a large number of cells into colloid 
material in one vicinity produces colloid masses or the so-called 
colloid cysts. Colloid substance is homogeneous or slightly gran- 
ular and is stained, by acid stains. It assumes an orange color 
when stained according to Van Giesen's method. 

Tissue Affected. — Epithelium is probably the only tissue 
in which colloid formation occurs. The thyroid gland is most 
commonlv affected. There is a degenerative change occurring 
in carcinomata that is similar to the colloid formation although 
it may be pseudomucin formation. McFarland states that col- 
loid casts occur in the uriniferous tubules, in. kidneys affected 
with chronic inflammation. Ziegler regards the prostatic con- 
cretions, of the human, that do not react to iodine, as colloid. 



220 VETERINARY PATHOLOGY. 

Effects. — The effects of colloid accumulation depend upon 
the extent of it. The exact function of the thyroid gland has not 
been determined but it is quite certain that the iodine compound, 
iodothyrein or thyroiodin is the active principle of the thyroid 
secretion. It is not known whether the thyroid secretion has 
:>ome action rron cell metabolism or neutralizes various poison- 
ous substances that result from metabolism or poisons intro- 
duced into the body from without. The colloid accummulations 
in goitre contain less iodine per given volume than the normal 
secretion, but the total quantity of iodine is materially increased 
resulting in circulatory disturbances, as rapid weak pulse, in- 
creased metabolic activity especially of proteids, increased secre- 
tions, irritability, etc. Diminished iodine production, as ob- 
served in mywioedema, is not common in colloid accummulation. 

SEROUS INFILTRATION. 

DEFINITION. 
ETIOLOGY— {Oedema'). 
APPEARANCE. 

Macroscopic. 

Microscopic. 
TISSUE AFFECTED. 
EFFECTS. 

Serous infiltration is a condition in which excessive quantities 
of lymph or serous fluid infiltrates the cells. 

In the anatomo-physiologic discussion of the cell, the nutri- 
ents were said to be obtained by specific selective action of the 
cells and by osmosis. Osmosis is probably the most important 
mode of passage of extracellular substances into the cell. 

In hydremia or other conditions in which cells are bathed by 
excessive quantities of fluid, there is a tendency for them to 
become hydropic. 

Serous fluid that enters the cells in serous infiltration is thin, 
watery and contains small quantities of proteids and salts. 

Etiology. — The cause of serous infiltration is an excess of 
serous fluids in the tissues. Serous infiltration is, therefore, an 
accompanying condition of oedema and the causes of oedema 
would likewise be the primary cause of serous infiltration. A 
second cause may be the impairment of the cells in which they 
are stimulated to imbibe more fluid. 

Appearance. — Macroscopis. — Because of the simultaneous 
occurrence of oedema and cellular serous infiltration and in 
view of the fact that oedema is so conspicuous, the serous infil- 
tration is not recognizable in gross examination. 



RETROGRESSIVE TISSUE CHANGES. 221 

Microscopic. — When examined in the fresh state the cells 
are enlarged, the extent of which depends upon the quantity of 
fluid imbibed. The infiltrated fluid accumulated in the cells 
appears as clear spaces or vacuoles. The vacuoles occur either 
in the cyto-plasm or the nucleus and in extreme cases, they 
occupy the entire cell and may even cause its rupture. 

Tissues Affected. — Practically all tissues are subject to 
serous infiltration. Those tissues in which oedema occurs are 
most frequently affected. Epithelium is quite frequently in- 
volved in serous infiltration because this tissue forms the sur- 
face of those structures affected with oedema. 

Effects. — The effects depend upon the extent and duration 
of the condition. Some vegetable cells are capable of imbibing 
fluid to a sufficient extent that they increase their size one hun- 
dred times. 

Animal cells cannot imbibe fluids to such an extent as vege- 
table cells without being rent asunder. After tke cells have 
been subjected to serous infiltration for sometime, the nuclear 
chromatin appears to dissolve and diffuse through the cell body. 
This necessitates an impairment of the cell activities. 



GLYCOGENIC INFILTRATION. 

DEFINITION.^ 

ETIOLOGY — (Disfitrbed carbohydrate metabolism). 

APPEARANCE. 

Macroscopic. 

Microscopic. 
TISSUE AFFECTED. 
EFFECTS. 

This is a condition characterized by the infiltration of exces- 
sive quantities of glycogen into cells that normally contain a 
limited amount of it or the infiltration of glycogen into cells 
normally glycogen free. 

The source of glycogen is not definitely known. Accord- 
ing to some physiologists, glycogen may be formed from either 
carbohvdrates or proteids. The digested carbohydrates are 
probably stored up in the form of glycogen, at least glycogen 
is readily converted into dextrose whenever carbohydrates are 
needed. Glycogen can be demonstrated in the normal liver cells, 
kidney cells, and in muscle cells, although it occurs in limited 
quantities. 

Glycogen is soluble in water and insoluble in alcohol, chloro- 
form and ether. Its presence in tissue may be demonstrated by 
smearing the tissue on a slide and allowing it to dry inverted, 



222 VETERINARY PATHOLOGY. 

over crystals of iodine. The glycogen appears as brownish areas 
in the cells. It may also be demonstrated by immersing in a 
mixture of four parts of alcohol and one part of tincture of iodine, 
sections that have been hardened in absolute alcohol, the glyco- 
gen assuming a port wine color. 

Pathologic glycogenic infiltration occurs in pus cells of suppu- 
rating processes. The blood cells, especially leucocytes, contain 
some glycogen in those animals affected with septic infection or 
sapremia. Thus horses afflicted with sapremia induced by punct- 
ure wounds of the foot show glycogenic infiltration, of the blood 
cells. In diabetes mellitus the liver and kidney cells are infil- 
trated with excessive quantities of glycogen. 

Etiology. — Disturbed carbohydrate metabolism is insepar- 
ably associated with glycogenic infiltration although the specific 
relation of disturbed carbohydrate metabolism and glycogenic 
infiltration is not known. Glycogenic infiltration has some asso- 
ciation also with certain infectious and inflammatory disturban- 
ces as well as tumor formations. 

Appearance. — Macroscopic. — Glycogenic infiltration does not 
produce lesions sufficiently characteristic to be recognized with- 
out the aid of a microscope. 

Microscopic. — The affected cells contain transparent colorless 
areas near the nucleus. If the specimen has been hardened in 
absolute alcohol, the areas of glycogen may be stained port 
wine color by four parts of alcohol and one part tincture of 
iodine. The areas are variable in size depending upon the ex- 
tent of the condition. In extreme cases the glycogen may be 
observed in the intercellular spaces. 

Tissues Affected. — Liver, kidney, muscle, and blood cells are 
most subject to glycogenic infiltration, the frequency in the order 
named. 

Effects. — The glycogen is readily reabsorbed provided the 
cause be removed. The condition being associated with other 
pathologic conditions, their removal becomes essential before 
the glycogenic infiltration can be overcome. 



RETROGRESSIVE TISSUE CHANGES. 225 

URATIC INFILTRATION. 

GENERAL DISCUSSION. 

DEFINITION. 

ETIOLOGY — Deficient uric acid secretion, 

APPEARANCE. 

Macroscopic. 

Microscopic — Needle like crystals. 
TISSUE AFFECTED— Articulations. 
EFFECTS. 

Uric acid is formed by the kidneys from urea and passes out 
normally with the urine. If not promptly eliminated, it com- 
bines with sodium carbonate of the blood to form sodium urate 
(quadriurate and biurate). The quadriurates are unstable but 
the biurates are quite stable. Uric acid and urates do not nor- 
mally exist as such in the blood of birds or mammals. The urin- 
ary excrement of birds is composed of urates but no urea. In 
birds the ureter terminates in the cloacum ; the kidney excretion,, 
which is almost solid in consistency, is thus mixed with the feces 
before it is eliminated from the body. This anatomic arrange- 
ment probably favors the resorption of uric acid. At any rate 
uratic infiltration is more common in birds than in any other 
domestic animal. 

Sodium urate is the usual compound found in uratic infiltra- 
tions and when examined miscroscopically appears as a feltwork 
of radiating clusters of needle like crystals. If urate of sodium be 
treated with a few drops of nitric acid, and then evaporated to 
dryness, and to the amorphous residue a few drops of ammo- 
nium hydrate be applied, the entire mass assumes a purple-red 
color, or if potassium hydroxide be applied, the mass becomes 
bluish-purple. 

Etiology. — Uratic infiltration is due to deficient excretion 
of uric acid by the kidneys. It may be caused by ligation of the 
ureters or by any obstruction to these ducts. An exclusive 
meat or other nitrogenous diet, sometimes produces uratic infil- 
tration in fowls. Old age is a predisposing factor. 

Appearance. — Macroscopic. — The phalangeal, metatarsal and 
tarsal joints are most frequently affected in fowls. In the begin- 
ning the condition is evidenced by a soft, painful, diffuse swell- 
ing becoming more circumscribed as it becomes larger. The skin 
over the affected area becomes thickened and scales off as the 
swelling increases in size. The nodular swellings ultimately 
rupture, the contents being buff colored and crumbling as it is 
discharged. Sometimes masses of the urates accumulate as 
small stones (tophi) under tendons, etc. The articular surfaces 
are frequently eroded. 



224 VETERINARY PATHOLOGY. 

Microscopic. — The needle like crystals of sodium urate, in 
addition to more or less detritus from necrosis of the tissue, is 
characteristic of sections or smears of tissues affected with uratic 
infiltration. 

Tissue Affected. — Articulations are the usual location of 
uratic infiltration, especially those in the metatarsal region. The 
skin and visceral organs may be affected. 

Effects. — The accumulation of the urate crystals in the artic- 
ulation, produces erosion of the articular surfaces, and thus 
interferes with movement. Tophi beneath tendons also produce 
disturbance of mobility. 



KERATOSIS. 

DEFINITION. 
GENERAL DISCUSSION. 
ETIOLOGY. 

Dessication of surface epithelium. 

Excess of intercellular cement. 
APPEARANCE. 

Macroscopic — Horny growths. 

Microscopic. 
TISSUE AFFECTED— Epithelium. 
EFFECTS. 

Epithelium becomes cornified thus forming the hard horny 
hoofs, horns and claws. The conversion of epithelium into horn- 
like substance (characteristic of the hoof) consists of a dehy- 
dration of the cells and the production of a glue like material 
that cements the dessicated cells together. The ergots and 
chestnuts in the skin of the horse are produced by the accumu- 
lation of dessicated cells cemented together. 

The cornified epithelium that characterizes keratosis varies 
from dried scales to dense horn tissue. 

Pathologic cornification is of rather common occurrence in 
the domestic animals. The skin covering the carpus of oxen fre- 
quently becomes materially thickened and cornified, one case 
having been observed in which the cornified mass accumulated 
until a projecting horn like structure some ten inches long and 
six inches in diameter at its base, was present. As a general 
condition it is observed in the skin of animals affected with ich- 
thyosis. 

Etiology. — Irritation appears to be a causative agent in 
keratosis. The condition may be a sequel of inflammation and 
sometimes occurs in scars. Whatever increases dessication of 



RETROGRESSIVE TISSUE CHANGES. 



225 



epithelium and stimulates the formation of excessive quantities 
of cellular cement favors keratosis. 

Appearance. — Macroscopic. — Keratotic accumulations appear 
like so much irregularly formed horn tissue. The resistance 
of the cornified epithelium varies according to the completeness 
of cornification. 




Fig. 119.- 



-Photograph of a Keratotic, horn-like growth removed froiu 
region of withers of an ox. 



Microscopic. — The cornified epithelium usually appears as 
a mass of debris, although in some instances there may still be 
evidence of cellular elements. The epithelial pearls of epitheli- 
omata probably represent a type of keratosis, — the pearls appear- 
ing as w^hirls of scale like elements suggesting the gross appear- 
ance of a section of an onion. 

Tissue Affected. — Epithelium is particularly affected. Some 
tumors are affected, especially epitheliomata. 

Effects. — The area involved is inconvenienced. If the en- 
tire skin is involved there may be secondary constitutional les- 
ions. 



226 VETERINARY PATHOLOGY. 



OSSIFICATION. 

PHYSIOLOGIC. 
PATHOLOGIC. 
ETIOLOGY. 

Irritation. 

Improper nutrition. 
APPEARANCE. 

Macroscopic — Osseous viasses. 

Microscopic — Osseous plates. 
TISSUE AFFECTED. 

Muscle. 

Arteries. 

Tumors. 
EFFECTS. 

Ossification, as in the formation of bone, is a normal process. 
The process consists in the formation of fibrous lamellae that 
are later calcified. Osseous bodies are sometimes formed in such 
structures as the falx cerebri and tentorium cerebelli. These 
osseous formations assume the shape of the original structures, 
and are called osteophytes. 

Pathologic ossification consists in the formation of a bone 
like substance in abnormal locations, as muscles, arteries, tum- 
ors, etc. 

Etiology. — Ossification probably results from chronic irrita- 
tion, improper circulation, or impoverished nutrition. 

Appearance. — Macroscopic. — Ossified muscle appears as a 
porous osseous mass. In an autopsy of a horse the flexor bra- 
chii muscle, was found to be a porous osseus mass, and appeared 
like cancillated bone. Muscle ossification is usually des- 
ignated myositis ossificans. An ossified falx cerebral or tentor- 
ium cerebellar osteophyte appears as irregular bony masses. 

Microscopic. — The porous osseous tissue formed in pathologic 
ossification is found on microscopic examination to consist of 
osseous plates surrounding irregular cavities. 

Tissue affected. — Muscle, arteries, connective tissue and tum- 
ors. 

Effects. — Ossification occurs only when the normal struct- 
ures have been practically destroyed. It represents a condition 
that is not reparable. 

For differentiation of this condition and osteomata see discus- 
sion of the latter. 



RETROGRESSIVE TISSUE CHANGES. 227 



CALCAREOUS INFILTRATION. 

DEFINITION, 
ETIOLOGY. 

Impaired circulation. 

Rickets. 

Intoxication, Mercury, etc. 
VARIETIES. 

Tissue Spaces — Calculi. 

Tissue. 
TISSUE AFFCETED. 
EFFECTS. 

Calcareous infiltration ii a condition in which lim^ salts are 
deposited in abnormal locations or excessive quantities are 
deposited in those tissues in which calcareous depositions nor- 
mally occur. 

In the formation of osseous tissue, certain definite quantities 
of lime salts impregnate the softer formative tissue, thus produc- 
ing typical bone. Considerable quantities of lime salts normally 
occur in the blood and lymph of the various animals. The urine 
of the horse, donkey, and mule frequently contains such large 
amounts of calcium phosphate that it is quite turbid when ex- 
creted. Excessive quantities of lime salt in solution predispose 
to calcareous infiltration as well as to calculus formation. 

The lime salt most frequently found in tissues affected with 
calcareous infiltration is the carbonate, though other salts of 
lime may be present as the phosphate and rarely, the sulphate. 
These salts are all insoluble in water, alcohol, ether and chloro- 
form, as well as most other solvents. The application of dilute 
acids usually cause excessive eft"ervescence because of the lib- 
eration of carbon-dioxide. 

Pathologic calcareous infiltration sometimes occurs in dense 
scar or cicatricial tissue as in extreme cases of poll evil, fistu- 
lous w^ithers or quittors ; in necrotic areas as tubercles of tuber- 
culosis in cattle and hogs ; in necrotic areas of arteries affected 
with atheromatous degeneration ; in inspissated pus ; in the sup- 
porting framework of the lungs producing pneumono-koniosis ; 
in the kidney ; and in other organs in chronic bichloride of mer- 
cury poisoning; in parasitic cysts, as the trichina cysts in hogs, 
and psorosperm cysts ; and in dead foetuses. 

Etiology. — Imperfect circulation.— Twhtvcnl^iV lesions (tubercles) 
are nonvascular and invariably become calcified sooner or later. Al- 
though tubercles are nonvascular, there is more or less enzy- 
motic action taking place resulting in the liberation of carbon 
dioxide; there are variable quantities of fluid containing lime 



228 VETERINARY PATHOLOGY. 

salts in solution filtering into the tubercles ; the liberated car- 
bon-dioxide combines with the soluble lime salts forming insolu- 
ble calcium carbonate which is deposited in the tissue thus pro- 
ducing calcification. Enzymotic action is also present in local 
areas of tissue, other than tubercular, that have recently become 
necrotic, as inspissated pus, thrombi, infarcts, necrotic areas in 
arteries, and there is also sufficient soluble lime salts present 
to combine with the carbon-dioxide liberated by the enzyms to 
form insoluble calcium carbonate, thus necrotic tissue becomes 
calcareous. 

Dense fibrous masses are frequently poorly nourished because 
of the obliterated vessels and occasionally become calcareous. 
Thus it is not rare to find calcareous centers in the dense fib- 
rous tissue of fistulous withers. 

Improper Food. — Food or water containing excessive quanti- 
ties of certain lime salts predispose to calculus formation and in 
some instances to the deposition of lime salts in tissues as the 
kidney and lung. 

Inhalation of air containing large quantities of lime or clay dust 
in suspension, results in their deposition in the alveoli of the 
lung, and infiltration into the framework of the lung producing 
the condition known as chalicosis. Horses and mules worked 
in and around cement plants, stone crushers, rock quarries, etc., 
are affected Avith pulmonary chalicosis and are more subject to 
pulmonary diseases than animals not so affected. 

There are probably some chemic substances, resident in the 
body which when increased or diminished favor the deposition 
of Ijme salts. It may be that the chemic reactions of a tissue is 
a factor of considerable moment in calcareous infiltration. 

Appearance. — Macroscopic. — Tissue affected with calcareous 
infiltration is hard, granular and gritty. When palpated, it is 
quite resistant and may be massive, but is more likely to be com- 
posed of small calcareous masses held together by variable quan- 
tities of soft tissue. It is gritty when incised or sawed and in 
some instances the tissue is so densely infiltrated that it is impos- 
sible to either cut it with a knife or saw, a chisel being required 
to break it asunder. Calcareous tissues are heavier than normal 
tissues. Tissue may be equally affected throughout or the calcar- 
eous material may be concentrated in small areas arranged con- 
centrically around a central mass or in lines radiating from a cen- 
tral point. The calcareous material may appear in spherical 
masses as in the tubercular lesions or in scales as in arteries 
affected with athermatous degeneration. The air cells and bron- 
chioles in the lungs of horses affected with chalicosis contain 



RETROGRESSIVE TISSUE CHANGES. 



229 



incrustation of scales of lime and the framework of the lung may 
be infiltrated with small gritty calcareous masses. 

Microscopic. — The calcareous material may be amorphous or 
crystalline and it may occur in the cells or between the cells. 
Cellular calcareous infiltration normally occurs in the cells of 
the pineal body and pathologically in kidney cells, nerve cells, 
etc. The calcareous granules or crystals are usually stained 
dark with hematoxylin and give the general impression that 
chromatolysis (fragmentation of the nucleus) had occurred. 




Fig. 120. — Atheromatous Degeneration, Aorta. 

a. Calcarious deposit in the tunica media. 



Calcareous material infiltrated between the cells may be amor- 
phous or crystalline and assumes the same stains and appears 
similar to the intracellular infiltrated lime salts. The calcareous 
material is soluble in dilute acids, except calcium sulphate, with 
more or less effervescence. 

Tissue Affected. — Necrotic tissues are most subject to cal- 
careous infiltration. Blood vessels, lung tissue, kidney tissue^ 
dense fibrous tissue, are also subject to calcareous infiltration. 

Effects. — Calcareous infiltration is a means of converting 
necrotic tissue into a noninjurious mass. Calcified tissue is prob- 
ably never regenerated because calcareous deposits are not -ab- 
sorbed. 



230 VETERINARY PATHOLOGY. 

CACULI. 

DEFINITION. 

ETIOLOGY. 

STRUCTURE. 

SHAPE. 

SIZE. 

NUMBER. 

COLOR. 

COMPOSITION. 

VARIETIES. 

Urinary. 

Salivary. 

Gastric. 

Intestinal. 

Biliary. 

Lacteal. 

Venous. 

Arterial. 

Calculi are accumulation in the body cavities, of min- 
eral matter precipitated from the body fluids, or they miay 
be mineral incrustations upon foreign substances in the body 
cavities. The mineral deposits formed within the tissues of 
the animal body, as calcified tubercules, etc., are calcareous in- 
filtration or tissue petrification. Calculi, however, may and 
frequently do, become attached to the tissue, surrounding them 
(phleboliths), and a calcified tissue may become separated from 
the surrounding structures (calcified necrotic tissue in fistula). 
Hence the two conditions, calculus formation and calcification, 
approximate each other closely and at times are not separable. 
Etiology. — The causes of calculus formation are not thor- 
oughly understood. The most probable cause is the supersatur- 
ation of the body fluids with salines. The fluids may become 
super-saturated either by an excessive production of the salines 
or diminished excretion of them. The lack of oxygen or an 
excess of carbon dioxide may cause the precipitation in body 
fluids, especially of calcium and magnesium carbonates. Fer- 
mentation of various juices may result in precipitation of a vari- 
ety of compounds. But why the precipitate should accumulate as 
a calculus is unexplained. It is a phenomenon cot understood. 
There are many predisposing causes that aid in the formation of 
calculi. The retention or delay in the excretion of fluids, especi- 
ally if they undergo any chemical change, are principal factors in 
calcular formation. Intoxication from mercury predisposes to the 
formation of urinary calculi. The presence of any foreign body, 
as particles of sand, desquamated cells, coagulated albumen, 
parasites, etc., upon which a precipitate may accumulate, is a 
predisposing cause. According to Ziegler all calculi have an 



RETROGRESSIVE TISSUE CHANGES. 231 

organic nucleus. But it seems possible and quite probable that 
particles of inorganic matter ai^e deposited upon an inorganic 
nucleus in the formation of calculi. 

Structure. — The structure of calculi varies. Homogeneous 
calculi are composed of layer upon layer of the same material 
and have the same appearance throughout. Heterogeneous cal- 
culi are laminated, i. e., they are composed of layers of different 
material and appear different in the succeeding layers. Calculi 
vary from finely granular masses (appearing as though many 
grains of sand had been fused into a mass) to lobulated masses 
(mulberry calculi) ; or thc}^ appear smooth as though they were 
molten mineral run into forms. 

Shape. — Calculi assume all conceivable shapes. Cystic calculi 
vary in form from spheres to jack straws, and even coral like 
bodies or stalactite calculi have been observed. Their form may 
be determined by their location. Thus renal calculi may assume 
the shape of renal tubules, renal pelvic calculi the shape of the 
renal pelvis. Intestinal calculi are usually more or less spherical 
in shape. Salivary calculi are ovoid. Calculi may be faceted 
when occurring in large numbers. 

Size. — The size of calculi varies from the finest sand-like 
grains to enormous accumulations. A 228-gram (7 oz.) cystic 
calculus was removed from a Jack, by Dr. McCasey, Concordia, 
Kansas. A 260-gram (8 oz.) cystic calculus was removed from a 
five-year-old Jack at the Missouri Valley Veterinary Association 
clinic in February, 1907. D'r. Z. C. Boyd, in 1906, removed from 
Steno's duct, in a horse, a salivary calculus weighing 125 grams 
(4 oz.). 

Number. — The number of calculi occurring in one animal is 
quite variable. There has been a case reported in which there 
were over 300 cystic calculi in one dog, although that is an un- 
usual number. 

Color. — The color of calculi is determined by their composi- 
tion. Thus biliary calculi are highly colored because of the bile 
pigment, bilirubin and biliverdin, that they contain. Enteroliths 
are usually colored from the intestinal contents. Arterioliths 
and phleboliths are colored with hemoglobin or some of its 
derivatives. Urinary calculi may be gray, brown, yellow, or 
even red, depending upon their composition. Salivary calculi 
may be chalk white or tinged with various colors. 

Composition. — A variety of chemical compounds are found 
in the various calculi. Urinary calculi may contain cystin, xan- 
thin, urates, oxalates, carbonates, phosphates, calcium, magnes- 
ium, etc. Cystin and xanthin urinary calculi are quite rare. 



232 



VETERINARY PATHOLOGY. 



Urates are common in renal tubular calculi, also in cystic calculi 
of dogs and cats. Carbonates predominate in cystic calculi of 
the horse and ox. Ammonium-magnesium-phosphate is the prin- 
cipal compound in cystic calculi of the sheep and hog. Urethral 
calculi are of the same composition as cystic calculi of the 




Fig. 121. — Group of Calculi, showing- a variety of shape. 



same animal. Preputial calculi are usually composed of car- 
bonates in the horse and of phosphates in the ox and sheep. 
Biliary calculi may be composed of carbonates or phosphates, but 
are more frequently composed of calcium biliverdin. Enteroliths 
may contain a large nucleus of fecal matter or hair which be- 
comes permeated and incrusted with calcium or magnesium car- 
bonates, phosphates, sulphates, or oxalates. Salivary calculi, 



RETROGRESSIVE TISSUE CHANGES. 



2ZZ 



arterioliths, and phleboliths are usually composed of the carbon- 
ates and phosphates of calcium and magnesium. Lacteal calculi 
are composed chiefly of phosphates. 
Varieties. 

Urinary Calculi are of frequent occurrence and may be con- 
veniently classified according to the location in which they 
occur. 

1. Renal tubular calculi are most common in dogs and cats, 
but may occur in horses, cattle and hogs. After formation they 
frequently pass into the pelvis of the kidney and the urine may 
v^ash them down through the ureter into the bladder and some- 




Fig. 122. — Photograph of a 7 ounce Cystic Calculus successfully removed from the 

bladder of a jack. 



times on out of the animal body. They may obstruct the tubule 
causing retention of urine with distension of the tubule and fre- 
quently cyst formation. 

2. Renal pelvic calculi are not rare, the pelvis of the kidney 
sometimes being completely filled with a calculus. This variety 
has been observed in the hog, dog, cat, horse, and sheep, the 
frequency in the different animals being in the order named. 
A 7-gram {% oz.) renal pelvic calculus Avas obtained in 1906 
from a horse used for dissection purposes at the Kansas City 
Veterinary College. G. H. Woolridge, of Dublin, describes a 
case of calculus formation in the renal pelvis of a horse (Veter- 
inary Journal for June, 1907) in which the entire kidney was 
practically replaced by the calculus. The results of calculi in 
the renal pelvis depend upon their extent. Complete obstruc- 
tion necessarily results in the retention of urine followed either 
by its resorption (producing uremia) or its accumulation (form- 



234 



VETERINARY PATHOLOGY. 



ing a cystic kidney). The former condition is common in dogs, 
the latter in hogs. 

3. Ureter calculi have been observed but are rare. 

4. Cystic or vesical calculi are the most common of all urin- 
ary calculi. Dogs and cats are quite subject to them, occurring 
more frequently in the older animals, but the puppy and kitten 
are not exempt. Bitches and castrated male cats are especially 
subject to cystic calculi. Jacks are frequently affected with 
cystic calculi, horses, goats, sheep and cattle less frequently. 
A cystic calculus 18 x 20 cm. (7x8 inches) was successfully 
removed from a 2-year-old colt by Dr. E. S. Fry, of 







^m^mj&m 






mmm 


■i 






■^ 




S^^K 


1 


1 








' 




1 


1 


i 
1 


I 






-.2: . 






mi. 












,>'S 



Fig. 123. 
Preputial calculus. 



-Urinary Calculi 

2. Renal pelvic calculi. 



Naperville, 111. Cystic calculi may cause no inconvenience or 
they may produce sufficient irritation to establish a severe cyS' 
titis. They may obstruct the urethral opening resulting in reten- 
tion of urine and rupture of the bladder. Frequently they become 
imbedded in the walls of the bladder, and may cause dilatation 
or pouching of its walls. Sometimes the calculi pass out of the 
bladder and become lodged in the urethra, resulting in retention 
of urine, difficult micturition, and usually urethritis. 

5. Urethral calculi are common in old dogs, also in the bull 
and ram, and have been observed in the horse. They occur in the 
urethra, in the beginning of the gutter of the os penis in the 
dog, usually in the first curve of the penis in the bull, just pos- 
terior to the meatus urinaris in the ram and at the ischial arch 



RETROGRESSIVE TISSUE CHANGES. 



235 



in the horse. They usually cause difficulty in micturating and 
may completely obstruct the urethra with the same results that 
are produced by occluding the urethral opening of the bladder. 
Urethral calculi may produce erosions of the urethra and sur- 
rounding tissues and thus, produce an artificial urinary canal 
through which the urine will be discharged, this is probably 
more common in male bovines, than in other animals. 
About 200 urethral calculi were observed in "the urethra of one 
steer by Dr. B. F. Kaupp. 

6. Preputial calculi sometimes occur in geldings, although these 
are more frequently accumulations of the secretion from the ad- 
jacent sebaceous glands. W. Williams reported cases in which 
there was formation of stalactite bodies in the prepuce of oxen 
and sheep that had been fed food material containing a large per 
cent of phosphates. A preputial calculus weighing 11 grams 
(Yg oz.) and another weighing 10 grams were obtained from a 
hog by a veterinary inspector. 

Salivary calculi occur most frequently in the horse, although 
they do occur in the ass, ox and sheep. Their formation depends 
upon the ingested water containing a large quantity of car- 
bonates of potassium, sodium and magnesium and the presence 
of calcium salts in the saliva. (Dr. J. M. Lawrence, Veterinarian 
U. S. Army, Fort Wingate, N. M., operated upon two horses, 
removing from Steno's duct in each a salivary calculus. In 
the center of one of these calculi an oat grain (nucleus) was 




Fig. 124. — Photograph of a Salivary Calculus removed from. Steno's Duct, horse. 



found upon which the deposit had taken place. This calculus 
weighed 19 grams (-/g oz.) The result of salivary calculi is 
to obstruct the outflow of saliva, the retention of which in the 
smaller ducts may cause inflammatory, degenerative or atrophic 
changes in the gland, and if the calculi are not removed the des- 
truction of the gland or the rupture of the duct and a salivary 
fistula. Tartar on dogs' teeth has an origin similar to that of 
salivary calculi. 



236 



VETERINARY PATHOLOGY. 



Gastric Calculi (gastroliths) occur in the paunches or reticula 
of cattle, sheep and goats. They are exceptionally rare in the horse 
and hog, and probably never occur in dogs and cats. 

Intestinal Calculi or enteroliths are found in the large intes- 
tine of the horse, especially those fed upon bran. These cal- 
culi are composed primarily of ammonio-magnesium phosphate, 
the magnesium phosphate being dissolved out of the bran by the 
acid of the gastric juice and uniting with nascent ammonia form- 
ing an almost insoluble phosphate. Enteroliths may be of enor- 
mous size, in some cases, weighing as much as ten kilograms 
(22 lbs.). These calculi are likely to cause erosions of the mucous 




Fig. 125. — Photograph of an Intestinal Calculus having a circumference 
of 12 inches and weighing 3 pounds. 



membrane as well as obstruction of the lumen of the intestine. 
Linch, of Albany, N. Y., reported a case in the Review, 1906, in 
which a calculus weighing 3.4 kilograms (7^ lbs.) was found. 
Gage reported a case in which a calculus weighing .9 kilo- 
grams produced fatal results. Hodgkins and Son of Hanley, Eng- 
land, recently obtained three enteroliths, each weighing 1.6 kilo- 
grams (3^ lbs.) from the intestine of a horse. 

Biliary Qalculi (Choleliths) are not rare in the domestic ani- 
mals. They vary from the size of la pea to a baseball, are tinted 
yellow, brown, red, green, or may be chalk white in color. Fre- 
quently they occur in large numbers, are variable in shape, and 
structure. They are usually composed of biliary pigments in 



RETROGRESSIVE TISSUE CHANGES. 



-Of 



combination with calcium, although carbonates and phosphates 
are common ingredients. Biliary calculi may form in the biliary 
collectinor tubules of the liver in the bile duct or in the sfall blad- 
der. The results of their presence depend upon their location 
and size. If they are small and cause no obstruction there will 
be no inconvenience from them. If thev are of a size that thev 
can be forced through the bile ducts they will produce severe 
colicky pains at the time of passage. They may be sufidcientlv 
large to obstruct the bile duct of some principal collecting tubule 
and produce a stagnation and resorption of bile_, resulting in 




Fig. 126. — Biliary Calculi, Ox. 

1. Showing- Facets. 3. Showins 

2. Showing Facets and Lamination. 



Crevice. 



various disturbances because of the presence of the bile in the 
blood. 

Lacteal Calculi (galactoliths) may be formed in the galacto- 
phorus sinuses, particularly of the ox. They are usually com- 
posed of calcium phosphate. 

Phleholiths or calculi in veins have been observed by Spoon- 
er in abdominal veins and by Simmonds in the jugular vein. 
The^r are probablv the result of calcification of thrombi which 
have later become detached from the vessel walls and are true 
calculi. They produce an obstruction in the vessels in which 



23S VETERINARY PATHOLOGY. 

they occur. They may be of slight significance or may cause a 
fatal termination, depending upon the importance of the vessel 
and extent of the collateral circulation or anastomoses. These 
calculi are usually composed of calcium compounds. 

Arterioliths are calculi formed in arteries. Their cause, for- 
mation, composition and termination being practically the same 
as that of phleboliths. 

Lithopedia are calcified foetuses. In extra-uterine foetation the 
foetus occasionally lives only for a short time. Dead extrauter- 
ine foetuses frequently become impregnated v^ith lime salts, 
producing the so-called lithopedia. Lithopedia may also occur 
v^ithin the uterus. This class of calculi is quite common in 
swine and some cases have been observed in cattle and sheep. 



CO'NCREMENTS. 

DEFINITION. 

ETIOLOGY. 

VARIETIES. 

Hair balls. 
^ Fecal matter. 

Bile. 

Pus. 

Milk. 

Cerumen. 

Concrements are accumulations of organic material in the 
cavities of hollow organs. Their effects are practically the 
same as the effects of calculi. Their formation depends upon the 
collection and massing together of organic substances derived 
either from the body in which the concrements occur or from 
some extraneous source. They may be hom.ogeneous or hetero- 
geneous in structure ; oval, spherical, or angular and faceted in 
shape, variable in size, color and number, (873 oat hair concre- 
ments were found in the great colon of a horse by C. Roberts, 
M. R. C. V. S.). They may be composed of hair, mucus, fecal 
matter, casein, inspissated pus or bile, ingesta of various kinds, 
etc. 

Hair Balls (Egagaropiles) are accumulations of hair into 
masses. They occur most frequently in animals that lick them- 
selves as the Ox and deer. Other animals are affected as the hog, 
dog and cat, also man, especially barbers, hair-sorters, hair-dress- 
ers, etc. Dr. A. Trickett observed a Persian cat that vomited 
a mass of hair >34"ii^ch in diameter and 3 inches long. Egagaro- 
piles vary in size from a pigeon's ^gg to a basket ball. They 
are in some cases simply masses of hair in others they are im- 
pregnated and incrusted with mineral substances, giving them 



RETROGRESSIVE TISSUE CHANGES. 



239 



the appearance of calculi. Hair balls incrusted with mineral 
salts taken from the deer by someone's grandfather or great- 
grandfather is the ordinary "mad-stone" in use at the present 
time. Recently a hair ball (bristles) completely filling the stom- 
ach was obtained from a hog slaughtered in a packing house. 
Hair balls are usually found in the abomasum or large intestines 
of the ox and in the stomach or large intestine of the hog. The 
presence of a hair ball produces the same effects that would be 
produced by any other indigestible body of the same size in the 
same location. 



Fecal Concrements. 

into compact masses. 



-The intestinal contents may accumulate 
These concrements interfere with the 




Fig. 127. — Hair Bans. 
(Egagaropiles.) 



240 



VETERINARY PATHOLOGY. 



movement of food-stuff through the canal and may completely 
obstruct it. Appendicitis in the human is frequently a result of a 
fecal concrement in the vermiform appendix. These concrements 
occur most frequently in the horse, dog and cat. They are usu- 
ally composed of cellulose in the horse, of bones and bone frag- 
ments in the dog and cat. The large intestine is the usual loca- 
tion of them in the horse and the small intestine in the dog or 
cat. ^laxwell reported a case in which alfalfa accumulated in 
the laro:e intestine of a horse, the concrements beinc^ trom 17^ 
to I'lYz cm. (T to 9 inches) in diameter. The fine hair of 
clover or oats frequently accumulates and forms concrements. 
The results of fecal concrements depend upon either mechanical 
interference in the passage of intestinal contents, erosion of the 
intestinal mucous membrane or perforation of the intestinal wall, 
or a combination of two or more of the above. 

Inspissated Bile. — If the outflow of bile is obstructed it will 
become condensed or inspissated to a degree depending upon 
the length of time of obstruction. Inspissation of bile frequently 
occurs. The animals most frequently affected are the ox and 
hog. An ox liver, containing several concrements composed of 
inspissated bile in the interlobular ducts, was recently presented 
to the Kansas City Veterinary College museum. Bile in this 
condition may form masses which in general appearance resem- 
ble biliary calculi. It is sometimes impossible to differentiate 
biliarv calculi from inspissated bile, and, in fact calculi are 




>:-niT»WjC» 



Fig. 12S. 
1. Inspissated pus from long abscess. 2. Inspissated pus. guttural pouch, horse. 



retro(;ressive tissue changes. 241 

frequently of secondary origin, the thickened bile forming the 
nucleus. The results of inspissated bile depend first upon the 
resorption of bile into the system and, second, upon the absence 
of bile in the intestine. 

Inspissated Pus. — Empyema sometimes terminates, when 
there is no surgical interference, in resorption of the liquor puris. 
after which the solid constituents frequently mass together, 
forming concrements. These concrements may form in any cav- 
ity in which the suppuration is slow going or chronic, provided 
the movement of the part is limited. Their formation has been 
noted in the guttural pouch. After formation they may become 
calcified. They are of little importance except as pathologic 
phenomena. 

Lacteal concrements result from the coagulation of the casein 
of milk and its accumulation in the galactophorous sinuses. 
These concrements occur in the cow and can usually be expelled 
through the lacteal duct by manipulation. 

Ceruminous concrements occur in animals in which the hair 
or wool extends far into the external auditory meatus. They 
are composed of cerumen and are the result of an excessive pro- 
duction or limited excretion of it. They may form into sufficient 
masses to completely occlude the external auditory canal and 
thus interfere with hearing. Concrements have been found m 
the bronchial tubes. Their formation depends upon the accu- 
mulation and condensation of mucus or purulent fluid. They 
may obstruct bronchioles and produce atalectasis. 

Prostatic concrements frequently occur in old dogs. They 
are present in many of the enlarged prostate glands. Thev con- 
sist of masses of accumulated colloid-like material. The results 
depend upon the pressure that they may exert. Thus there may 
be an obstruction to the outflow of urine. 



PIGMENTARY CHANGES. 

Physiologic pigmentation is variable. The color and extent 
of pigment varies in different animals and in the same animal 
under different conditions. All physiologic pigmentation is the 
result of deposition of hemoglobin or some of its derivatives. 

The skin of animals is usually extensively pigmented, with 
the exception of albinos and some white skinned animals not 
albinos. The production of the cutaneous pigment is not well 
understood but probablv results from metabolic activity of the 
deeper layers of epidermal cells. Because of the intense cutan- 



242 VETERINARY PATHOLOGY. 

eous pigmentation of animals, erythema, hemangiomata and other 
pathologic processes are not as evident as like conditions in the 
human. The excessive cutaneous pigmentation protects the skin 
from the injurious influences of sunlight. 

Hair, w^ool, fleece, fur and feathers are variously colored, the 
color depending upon the soluble pigment in the cortical portion 
of the cutaneous appendages. The color of the skin is usually 
an index to the color of the hair or similar epidermal appendages. 
The color of hoofs, horns, and clav^s is probably dependent upon 
cutaneous pigment. 

Voluntary muscle tissue is pigmented with varying quanti- 
ties of hemoglobin, excepting the so-called white meat of fowls 
(the sternal muscles and muscles of the pectoral arch). The 
pigmentation of the voluntary muscles varies in the different 
animals. The equine muscles are the most intensely red, the 
intensity of pigmentation in the muscles of other animals being 
in the following order : bovines, ovines, porcines, canines, felines. 
The flesh of duck and quail and the dark m.eat of other fowls is 
darker even than equine muscle. Heart muscle is very dark in 
color because of the excessive quantities of pigment. Gizzard 
muscle is intensely pigmented. Involuntary muscle of all ani- 
mals is very light in color, because of the limited quantity of 
pigment contained. The significance of the pigmentation of 
muscle is not known, possibly the hemoglobin of the muscle cell 
has some important metabolic function. 

The mucous membrane, particularly of the mouth, is fre- 
quently pigmented. The buccal mucous membrane of the sheep 
and dog is often black. The uterine mucous membrance of 
the bitch is occasionally quite black as a result of pigmentation 
derived from the uterine glands, and no doubt is indirectly a 
derivative of hemoglobin. 

Bones, especially the internal portion of the articular extremi- 
ties, are frequently pigmented from the red marrow that occupies 
the spaces in the cancellous bone. 

The liver and spleen are naturally deeply pigmented because 
of the excess of free hemoglobin in those organs. The kidney 
also appears pigmented, probably because of the excess quantity 
of blood contained in it. The choroid tunic of the eye is deeply 
pigmented with a substance not unlike melanin, the purpose of 
which is to absorb rays of light. 



RETROGRESSIVE TISSUE CHANGES. 243 

EXCESSIVE PIGMENTATION. 

(Hyperchromatosls.) 

DEFINITION. 
ETIOLOGY OR SOURCE. 
Hematogenous. 

Hemoglobin. 

Hemosiderin. 

Hematoidin. 
Hepatogenous. 

Bilirubin. 

Biliveridin. 
Cellular. 

Suprarenal — Addison s disease. 

Tumor — Melanin. 

Pregnancy. 

Freckles. 
Extraneous. 

Pneiimonokoniosis. 

Anthracosis — Carbon. 

Siderosis — Iron. 

Chalicosis — Lime. 

Kalinosis — Clay. 

A rgyriasis — Silver. 
TATTOO. 
EFFECTS. 

Excessive pigmentation, also known as pigmentary infiltra- 
tion, is a pathologic condition characterized by the presence of 
an excess of pigment in the tissues. Pathologic pigmentation is 
quite common. Icterus, melanosis, and anthracosis are types 
of pathologic pigmentation. This condition may be congenital 
as melanosis maculosa of calves, or it ma}- be acquired as in 
icterus. 

Etiology. — In pathologic pigmentation the coloring matter 
may be derived from internal sources^ as blood, bile and cells, or 
from external sources as coal dust, silver, lead and various pig- 
ments. 

Blood. — Pigmentation as a result of deposition of hemoglobin 
of the blood is designated hematogenous pigmentation. Hemo- 
globin is the principal hematogenous pigment, although hemo- 
siderin and hematoidin, both derivatives of hemoglobin, are of 
some importance. 

Hemoglobin is the normal coloring matter of the red blood 
cells and muscle. It constitutes about 90 per cent of the solids 
of red blood cells. It is a compound proteid and exists only in 
combination with lechithin. Hemoglobin splits up readily into 



244 



Veterinary pathology. 



globin and hemochromogen, the latter combines with oxygen to 
form hematin. 

Hemoglobin is liberated from the red blood cells in all condi- 
tions in which there is rapid destruction of these cells, as in tick 
fever, anthrax, hemorrhagic septicemia, toxic doses of chlorate 
of potassium, lead poisoning, etc. A portion of the liberated pig- 
ment is eliminated by the liver and kidneys, thus excessive quan- 
tities of bile and bloody urine (hemaglobinuria) are a feature of 
tick fever, lead poisoning, etc. The liberated hemoglobin not 
eliminated from the body is deposited, especially in the vessel 
walls, but ultimately diffuses into the lymph and infiltrates prac- 
tically all tissues. Post-mortem staining is the result of hemo- 
globin deposition into the dependent tissues. Hemoglobin is 
also liberated from muscle tissue in azoturia and other diseased 
conditions of m.uscle. The hemoglobin liberated from muscular 
tissue is disposed of in the same way as that derived from red 










'••-<\Y-^ 







Vl IS. 



Fig. 129. — Haemnosiderin Pisnientation. 

a. Tubules containing deposits of haemosiderin in the cells. 

b. Normal kidney tubules. 



RETROGRESSIVE TISSUE CHANGES. 245 

blood cells. Hemoglobin pigmentation, the results of bruising, 
is common in the superficial tissues of animals slaughtered im- 
mediately after shipping. 

Hemosiderin is a derivative of hemoglobin. It is yellowish 
brown in color, is insoluble in water, alcohol, ether, chloroform, 
dilute acids and alkalies. It contains iron and gives the typical 
iron reaction with potassium ferrocyanid. Hemosiderin is ihe 
common pigment observed in tissues that have been previously 
stained with hemoglobin. Extravasated blood observed in pete- 
chiae and hematomata appear as typical hemoglobin pigmenta- 
tion for a few days, after which the hemoglobin is converted into 
hemosiderin and the affected parts become a yellowish brown. 
Hemosiderin pigmentation is observed in tissues of animals that 
have been bruised three or four days prior to slaughter. It is 
also observed in post-mortem examinations of animals that have 
been affected with diseases accompanied by hemorrhages for a 
period of three to five days, as purpura hemorrhagica, acute tick 
fever, anthrax, etc. Hemosiderin pigmentation is of common 
occurrence in tumors. 

Heniatoidin is an iron free pigment, probably derived from 
hemosiderin. It is soluble in chloroform, but is insoluble in 
water, alcohol and ether. It occurs in rhombic crystals and is 
occasionally observed in old hemorrhagic foci. 

Blood pigments, hemoglobin, hemosiderin, and hematoidin 
are deposited in the cells and intercellular substances. The pig- 
ments are removed by solution and resorption of the dissolved 
pigment or by leucocytes which incorporate the insoluble pig- 
ment granules and carry them out. 

Blood pigmentation has little effect upon the tissue in which 
deposition occurs, but the flesh of food producing animals is 
usually condemned when pigmented because of its unsightly 
appearance. 

The deposition of a brownish or blackish pigment in bones 
(ochronosis) is occasionally observed in the carcasses of cattle 
which were apparently in good health. The cause of this pig- 
mentation is unknown. It probably does not injure the tissues 
or the meat for food, but such meats are usually condemned be- 
cause of their unsightly appearance. Another brownish pig- 
mentation of muscular tissue (xanthosis) is associated with mus- 
cular atrophy or disease of the suprarenal bodies. This condi- 
tion is of no consequence except public sentiment prevents the 
sale of such meat. 

Bile pigmentation results from the resorption of bile and its 



246 



VETERINARY PATHOLOGY- 



deposition in the tissue. Bile pigmentation is designated hepa- 
togenous pigmentation and the condition produced is commonly 
known as icterus or jaundice. Obstruction of the bile duct or 
any of its radicles by pressure, duodenitis, calculi, etc., will result 
in retention of the generated bile which is later resorbed into 
the blood. Destruction of considerable numbers of liver cells or 
diminution of their function may possibly result in the retention 
in the blood of those products that are normallv converted into 
bile, and thus produce a hematogenous icterus. Excessive pro- 
duction of bile, as in acute tick fever, is frequently accompanied 
by resorption of some of the bile and its deposition throughout 
the body, thus producing a generalized icterus. 

Bile staining is most evident in the conjunctiva and ocular 
sclera of the living animal where it produces a lemon or greenish 
yellow discolorization. If resorption of bile is very extensive 
it may appear in the urine. In carcasses, biliary pigmentation 
is most evident in the adipose tissue, especially the subcutaneous 
fat, although it is usually well marked in the subserous fat and 
may be detected in the lymph nodes, spleen, kidney and muscu- 
lar structures. 

The bile may be deposited in the cells or between the cells 
as greenish-yellow amorphous granules. The granules are read' 
ily soluble in alcohol, hence they are best detected in frozen sec- 
tions. 



-c\ 




Fig. 130. — Icterus affecting lymphatic tissue. 
a. Normal tissue. b. Deposit of bile pigment. 



KETtfOGRESSIVE TISSUE CHANGES. 147 

The effects of resorption of bile are variable. The tissues are 
discolored ; there ma}- be pruritus, as the bile appears to act as 
an irritant on nerve endings; putrefactive changes may occur in 
the intestine, and the heart may be depressed. Other inconstant 
symptoms may appear, especially if the quantity of resorbed 
bile is large. 

Cells. — Aside from hematogenous and hepatogenous pigmenta- 
tion the products of certain body cells become a factor in hyper- 
chromatosis. 

The principal pigment produced by cellular activity is mel- 
anin. JMelanosis maculosa is a congenital, cutaneous, patnologic 
pigmentation of calves resulting from the excessive production 
of melanin bv cutaneous cells in certain areas. 

Melanotic deposits are of common occurrence in the various 
glandular tissues, especially the liver, kidney, and suprarenal 
glands. The deposits in the glandular tissue may occur in the 
cells or intercellular spaces, and may appear as irregular yellow- 
ish-brown or black masses. Melanin may occur in the form of 
fine granules or be flocculent. Black kidneys are occasionally 
observed, in abattoirs, especially in hogs. These usually result 
from deposition of delicate, flocculent masses of melanin in the 
kidney cells. 

Melanosis is of most frequent occurrence in white animals, 
although it has been observed in Aberdeen angus cattle, red 
short horns, black and bay horses, a.nd black and red hogs. 

Melanotic tumors are pigmented with melanin. The melanin 
may be a product of the tumor cells or of the adjacent tissue 
cells. The principal melanotic tumors are the melano-sarcomata, 
although there may be a benign melanotic tumor called a mel- 
anoma. 

In a disease of the suprarenal capsule in the human (Addi- 
son's disease) there is a peculiar bronzing of the skin. This con- 
dition has not been noted in the domestic animal, probably be- 
cause of the dense pigmentation of the skin. It is thought to be 
a form of melanosis. 

■A pigmentation has been noted in atrophic tissues, especially 
atrophied muscles. The pigment of atrophic muscles may be 
the result of disturbed cell metabolism or it may result from con- 
centration of the pigment, because of the diminution in the size 
of the cells. Brown atrophy of the heart is a condition in which 
pigmentation is prominent. 

Freckles are pigmented areas of the skin in the human, the 
result of cutaneous cellular action. Because of the intense pig- 



248 VETERINARY PATHOLOGY. 

mentation of the skin in domestic animals, freckles are not easily 
observed, except in white animals. 

Pregnancy in the human is frequently accompanied by local- 
ized pigmented cutaneous areas. Such areas have not been re- 
corded in domestic animals. 

Aside from the blood, bile and cellular activities, pigments 
may be introduced into the body from without. 

The most common external substance that produces pigmen- 
tation is carbon. The most extensive pigmentation by carbon 
is in the lung, producing the condition known as anthracosis. 
Anthracosis is a common condition in the lungs of animals used 
in and around coal mines, in cities in which there is large quan- 
tities of coal smoke, in cats and other pet animals confined in 
coal bins, engine houses, etc. The inhaled carbon is largely ex- 
creted in the mucus discharged from the respiratory tract, al- 
though some of it is deposited in the epithelium of the air cells, 
and ultimately may be found in the interstitial tissue of the lung. 
Anthracosis apparently produces little harm unless it is exces- 
sive, when it predisposes to inflammatory disturbances. When 
examined in gross the lungs vary in color from a gray to a deep 
black. Microscopically small particles of carbon may be observed 
in the cells and intercellular substances of the lung tissue. 

Argyriasis is a condition in which silver is deposited in a tissue. 
After the silver is deposited it is combined with sulphur, thus 
forming silver sulphid, which is brownish black and imparts a 
similar color to the tissue. Argyriasis is not common in animals 
except those used in and around silver smelters or as a result of 
the application of some silver preparation to the tissues. 

Siderosis is a condition in which iron is deposited in a tissue. 
Iron, like silver, usually combines with sulphur, forming the 
sulphid, which is brown or black in color. Siderosis is not 
common in domestic animals, except in the intestinal epithelium 
of animals that have been medicated with iron preparations. 

Hydrargirosis is a condition resulting from the deposition of 
mercury in a tissue. This condition is present in the intestinal 
mucosa after medication with calomel or other mercury prepara- 
tions. The mercury sulphid, which is brown or black in color, 
is the usual pigment in hydrargirosis. 

Flumbosis is a term applied to pigmentation with lead. This 
form of pigmentation may be evident in the intestine in chronic 
lead poisoning. It appears as a bluish black pigment. 

Tattooing is the introduction of insoluble pigments into tissues. 
In tattooing, the tissues are first punctured or injured, after 
which some insoluble pigment is introduced into the w^ounds. 



RETROGRESSIVE TISSUE CHANGES. 249 

Some of the pigment is carried out by leucocytes and some of it 
is entangled in the cicatrix of the healing wound, where it re- 
mains permanently. Tattooing is a very valuable means of 
marking stock, as it gives a positive means of identification. 
Registered cattle, horses, sheep, hogs, dogs, etc., are tattooed in 
the ear, and fowls on the legs. The wound is made with an instru- 
ment similar to a hog ringer, in which slugs containing needle 
points arranged in the form of figures or letters are used. This 
instrument is used to punch holes into the inner surface of the 
external ear, immediately after which carbon is rubbed into the 
wound. When the wounds are healed, the tattoo may be easily 
observed. 

Effects. — Excessive pigmentation of a tissue or tissues is of 
little pathologic significance. Pigmented tissues are probably 
not hindered in their physiologic activities, excepting in so far 
as the cause of the pigmentation is an etiologic factor in the dis- 
turbance of the functioning of a part. Icteric pigmentation is of 
consequence because of the action of the bile upon nerve cells. 

Pigmentation, especially Avhen excessive, is a basis for the 
condemnation of meat and meat products because of public sen- 
timent. 



ABSENCE OF, OR DIMINISHED PIGMENTATION. 

(Hypochromatosis.) 

Visible pigmentation may be less than normal, and in some 
instances there is a complete absence of pigment. Areas con- 
taining less pigment than normal and depigmented areas are 
permanently Avhite in color, as they are not affected with sun- 
light or any other conditions that tend to produce pigmentation. 
This condition may be of antenatal or postnatal origin. 

Etiology. — Antenatal absence of, or diminished pigmentation/ 
may be inherited or it may be caused by disturbances of the 
embryonic cells that produce normal pigmentation. Postnatal 
absence of, or diminished pigmentation is usually the result of 
disease in which areas of tissue have been destroyed and later 
substituted by cicatricial tissue. 

The total absence of pigment (achromatosis) is not of com- 
mon occurrence, being most frequent in rabbits, birds and rats 
(albinos). An albino is an animal devoid of cutaneous and chor- 
oid pigment, the condition being inherited or congenital. The 
animals thus have white skin and usually white hair and their 
eyes are pink or red because of the absence of choroid pigment, 



250 VETERINARY PATHOLOGY. 

the blood being ob'served through the transparent ocular struc- 
ture. The so-called ''Wall-eyed" horses have little if any pig- 
ment in the choroid tunic, and frequently they have depigmented 
localized cutanveous areas. 

Depigmentation is probably never generalized. Permanent 
localized depigmentation, leucoderma or vitiligo, is a character- 
istic symptom affecting the external genitals of horses afflicted 
with dourine. 'It is also observed in cicatrices resulting from 
burns or extensive operative procedure. Surgeons usually make 
incisions in an oblique direction in order that the hair in the ad- 
jacent skin may cover the scar. Scars are usually devoid of hair, 
and when hair is present it may lack pigment. The application 
of some medicaments on the skin of some animals causes the 
hair to lose its pigment. 

Temporary depigmentation is evident after an attack of coi- 
tal exanthema, vaginitis accompanied by an ichorous discharge, 
and by many other conditions characterized by erosion or necro- 
sis of cutaneous tissue. 

Effects. — The absence of pigment is of no serious conse- 
quence except in some animals. Hogs that are white skinned 
cannot be raised in some localities because of the effects of the; 
sunlight. Depigmentation of the choroid is also of some conse- 
quence, because the eye is exposed to the effects of excessive, 
light. 



CHAPTER IX. 
NECROSIS AND DEATH. 

NECROSIS. 

DEFINITION. 
ETIOLOGY. 

Suspended nutrition. 
Thermic. 

Burning. 

Freezing. 
C hemic. 
VARIETIES. 

According to cause. 

Inanition. 

Thermic. 

Cheniic. 
According to character of necrotic tissue. 

Coagulation. 

CoHiquation. 

Caseation. 

Gangrene. 

MummiUcation. 
Miscellaneous. 

Senile. 

Fatty. 

Focal. 

Jack-sores. 
TISSUES AFFECTED. 
DISPOSITION OF NECROTIC TISSUE. 
Absorption. 
Exfoliation. 
Encapsulation. 
Sequestration. 
EFFECTS. 

Necrosis is local death. It is death of a part of the living body. 
The term necrosis is applicable to the death of any kind of tissue,, 
glandular, muscular, osseous, etc. Necrosis is usualh^ a rapid 
process, that is, it is sudden death of a part. Death of a cell or 
a group of cells that have been previously affected with degen- 
eration, i. e., a slow or lingering death, is termed necrobiosis. 
Caries is a term used to designate necrosis of dentinal or osseus 
tissue. 

Cells are constantly worn out and destroyed in physiologic 
active tissues. The physiologic destruction of cells is not usu- 
ally thought of as necrosis although the cause and manner of 
death may be similar, and there may be no difference in the ap- 
pearance of cells destroyed by physiologic and pathologic pro- 
cesses. 

251 



252 VETERINARY PATHOLOGY. 

The term necrosis is applicable to the pathologic death of a 
single cell, although such a limited necrosis is rarely recognized. 
Clinically necrosis is usually not noted except when the area is 
sufficiently large to observe with the unaided eye. 

All tissues of all animals are subject to necrosis, and it may 
occur upon a surface or in subsurface structures. Bursattae is 
a disease characterized by necrosis of the skin. Necrotic stoma- 
titis, a disease in puppies, calves and pigs, is accompanied by 
necrosis of the buccal mucous membrane. Tuberculosis, glan- 
ders, actinomycosis, and caseous-lymph-adenitis are diseases in 
which there is surface or subsurface tissue necrosis. 

Etiology. — Necrosis may be primary but it is more fre- 
quently secondary. Secondary necrosis is a sequel or result of 
some other pathologic process, as hemorrhage, oedema, throm- 
bosis, anemia, hyperemia, inflammation, degeneration, infiltra- 
tion and infection. 

Primary necrosis is the result of; (1) obstructed nutrition; 
(2) chemic substances ; (3) temperature variations. 

Obstructed nutrition. — A tissue or part, from which' nutri- 
tion is entirely obstructed, will die after all the available nutri- 
ents have been consumed. 

Nutrition may be obstructed from a part by some mechanical 
means. An occasional result of mechanically obstructed nutri- 
tion is observed in dogs in which a rubber band has been placed 
upon a leg, an ear, the tongue, or the tail, the circulation being 
thus obstructed the part distal to the rubber band soon becomes 
necrotic. The improper adjustment of bandages, especially when 
used to support fractures, is frequently a cause of necrosis. 

Tumors, cysts, abscesses and other pathologic enlargements 
may exert sufficient pressure to obstruct circulation and produce 
necrosis. Fractures and herniae may mechanically occlude blood 
vessels and result in necrosis. The seriousness of omental 
hernia or, in fact, any hernia, is due, to the fact that the vessels 
supplying the hernied structures are occluded, resulting in ne- 
crosis and the absorption of the products of the necrotic tissue. 

The plugging of a terminal vessel by a thrombus or an em- 
bolus (infarction) produces necrosis if collateral circulation is 
not established. Thrombo-embolic colic is a condition usually 
caused primarily by the larvae of the Strongylus armatus enter- 
ing and producing a parietal thrombus in the anterior mesen- 
teric artery, fragments of the thrombus become detached, pass 
down to and occlude the terminal mesenteric arteries, resulting 
in ischemia of the walls of the intestine, and if the circulation 
is not soon established the ischemic area becomes necrotic. 



NECROSIS xVND DEATH, 



^OJ 



A part or organ separated from the remainder of the body 
undergoes necrosis sooner or later, the time depending upon the 
condition of the tissue and the temperature in which the sep- 
arated portion is kept. Maceration and bruising produces ne- 
crosis to a varying degree, depending upon the extent of the in- 
jury. 




Fig. 131. — Photograph showing Necrosis above the foot of a horse. 

Chemic substances. — Certain 'chemic substances as phenol, 
arsenic, mercury bichloride, strong solutions of the caustic alka- 
lies and mineral acids, as well as the products of a large number 
of bacteria, are tissue destroyers. Phenol abstracts water from 
all cells to a sufficient extent to destroy their vitality, and it pro- 
duces a rapid disintegration of red blood cells. Arsenious tri- 
oxide is frequently applied on tumors because of its erosive 
action. Bichloride of mercury combines with the cell albumins, 
forming albuminate of mercury, thus inhibiting the cell action, 
and when all of the cell albumin is combined the cell is de- 
stroyed. The caustic alkalies and mineral acids coagulate the 
cell albumin or abstract the cell water, thus destroying them. 
The Bacillus necrophorous produces chemic substances that 
cause coagulation of the cell protoplasm (coagulation necrosis). 



254 



VETERINARY PATHOLOGY. 



De Schweinitz has described a chemic substance produced by 
the Tubercle bacillus, as necrotic acid, which is thought to pro- 
duce necrosis in tubercular lesions. The toxin of the diphtheria 
bacillus produces focal necrosis in practically all tissue in an 
individual afflicted with diphtheria. The products of pyogenic 
bacteria produce marked tissue destruction. 

Chemic substances produce necrosis by coagulation of the 




Fig. 132. — Bacillus Necrophorus — Pleomorphic form. 



albumin by dehydration or by the formation of new cell com- 
pounds, thus inducing metabolic disturbance and cell death. 

Temperature variations. — All active cells have a maximum 
and a minimum temperature. Thermic variations beyond these 
means are injurious and destructive if the variation is extensive. 
The high temperature causes coagulation of the cell protoplasm 
(cloudy swelling), which, if extensive, destroys the cells. 
Necrosis resulting from burning is of common occurrence. Low 
temperature is not as rapidly destructive as high temperature. 
Freezing produces necrosis of the tissues of warm blooded ani- 
mals, probably because of cell disintegration induced by the for 
mation of ice in the cells. 

Types or Varieties of Necrosis. — Several factors may be used 
as the basis for the classification of necrosis. 

Etiology. — According to the cause, necrosis may be : a. In- 
anition necrosis, b. Thermic necrosis, c. Chemic necrosis. 



NECROSIS AND DEATH. 



255 



Inanition necrosis is that type resulting from obstructed 
nutrition. As an example of this type may be mentioned the 
necrosis of the scrotum and its contents in rams induced by 
placing a rubber band moderately taut around its upper portion. 









Fig-. 133. — Photcgraph of the Ergot of Kye. 

This is a method frequently resorted to in the castration of old 
rams. Bed sores observed in the superficial structures in ani- 
mals afflicted with diseases that cause them to constantly assume 
the decubital position, are the result of obstructed nutrition in- 
duced by pressure upon the nutrient vessels or thrombic forma- 
tion secondary to bruising. 

Thermic necrosis results from exposure to extreme tempera- 
tures. Thus necrosis of cutaneous tissues is of common occur- 
rence in animals as a result of conflagrations or undue exposure 



256 



VETERINARY PATHOLOGY. 



to the solar heat rays or thermo-cautery. Necrosis induced by 
freezing is very common in calves, pigs, and chickens, in the 
temperate and frigid zones. 

Chemic necrosis is represented by the extensive destruction 
of the buccal, oesophageal, gastric, and intestinal tissues induced 
by the ingestion of lye. Corrosive sublimate and arsenious tri- 
oxide destroy the mucous membrane and frequently the deeper 
tissues of the alimentary tract in animals poisoned with these 
agents. 

Location. — Necrosis may be surface or subsurface. Surface 




Fig-. 134. — Ergot Poisoning in Cattle. Photograph by Dr. W. T. Spencer. 
Sloughing- above the feet. 2. Sloughing of the ends of the tails. 



necrosis may be of the skin, mucous or serous membranes. Sub- 
surface necrosis may be of any tissue, muscle, bone, glandular, 
etc. 

Nature or condition of the necrotic tissue. 

1. Coagulation necrosis. — This type of necrosis is character- 
ized by the coagulation of the necrotic tissue. It is the result of 
the presence of some enzym that produces the formation of fibrin 
or some allied substance. Coagulation necrosis is evident in the 
coagulation of blood and inflammatory exudates. The exudate 
in fibrinous inflammation (croupous and diphtheritic) usually 
becomes firmly coagulated. On the other hand, coagulation is 
rarely observed in collections of lymph, as in ascites, etc. The 
necrotic tissue in anemic infarcts, especially in the kidney, is 
sometimes coagulated. 

2. Colliquation necrosis. — The condition resulting from solu- 



NECROSIS AND DEATH. 257 

tion of a substance or surface area of necrotic tissue is colliqua- 
tion. Solution of the necrotic tissue is the result of enzyms 
that dissolve or digest the dead tissue. Suppurative processes 
(as abscess formation, etc.), are examples of this type of necro- 
sis. Liquefication of anemic infarcts, inflammatory exudates 
and thrombi, with or without the formation of cysts, is colliqua- 
tion necrosis. In the brain of horses that have died of the so- 
called blind staggers areas are found containing liquefied nerve 
tissue. 

3. Caseation necrosis. — When the fluid is absorbed from li- 
quefied necrotic tissue, the remaining solids may become cheese- 
like, thus producing the condition known as caseation. Caseation 
may be primary, but it is more frequently secondary to liquefying 
necrosis. Caseous material is granular, soft or crumbly in con- 
sistency. Caseation is characteristic of the typical lesion of cas- 
eous-lymph-adenitis in sheep and goats. Liquefaction precedes 
caseation in this disease. Tubercular lesions, especially in the 
bovine, is characterized by caseation, although they later become 
calcified. Necrotic centers of a caseous nature are observed in 
the lesions of bursattae. 

4. Mummifying necrosis (mummification, dry gangrene). — 
Necrotic tissues superficially located may becom.e dessicated, thus 
producing the condition known as mummifying necrosis. This 
type of necrosis occurs upon a surface that is freely exposed to 
air and of tissues in which there is little moisture. The ear, tail 
and hoof lesions, characteristic of ergotism, are the most typical 
examples of mummifying necrosis. In ergotism, the lesions are 
produced by constriction of the arterioles. This in turn in- 
creases blood pressure, and, consequently, the work of the heart. 
This ultimately results in the diminution or complete absence of 
blood from the extremities, and the latter sooner or later become 
necrotic. The necrotic tissue, as ears, tails, etc., in animals 
affected with ergotism become mummified because blood is prac- 
tically shut off from the affected parts and the contained moist- 
ure soon evaporates, for they are freely exposed to the air on 
two or more surfaces. Frozen tissues may become mummified. 
The umbilical cord in new born animals undergoes mummifica- 
tion. 

5. Gangrene. — By the laity, the term ''gangrene" is used to 
designate any type of necrosis, and by some medical men it is 
used to signify death of soft tissue en masse. Gangrene is that 
type of necrosis characterized bv putrefaction of the necrotic tis- 
sue. Gangrene invariably occurs in tissues in which there is a 
good supply of moisture, as in a tissue affected with venous con- 



258 



VETERINARY PATHOLOGY. 



gestion, and usually occurs upon a surface because infection is 
more likely to occur there. Parenchymatous mammitis of the 
bovine is frequently succeeded by necrosis and putrefaction of 
the necrotic tissue (gangrene). Gangrenous pneumonia is not 
uncommon and may be the result of embolic metastasis of organ- 
isms from septic metritis, etc., or it may be induced by medica- 
ments introduced into the lung. 
Miscellaneous. 

1. Senile Necrosis. — This is a type of necrosis occurring in 
old age. It is not uncommon in old dogs and aged horses, and 
is usually the result of inelasticity of the arteries and an insuffi- 
cient supply of nutrition. 

2. Fatty Necrosis. — This is a condition characterized by the 




Fig. 135. — Multiple Fatty Necrosis. 

Pat cells undergoing disintegration, because of Saponification. 



conversion of fat into fatty acid and glycerine, that is, saponifica- 
tion of fat. The name fatty necrosis is a misnomer, as the condi- 
tion is not necrosis. It should be called saponification of fat. In 
fact, a fully developed fat cell represents that amount of stored, 
available food, and there is in reality no vitality in the cell, and 
necrosis in dead tissue is not conceivable. Again, the real exist- 
ing condition is saponification of the fat, not necrosis. The prob- 
able cause of fatty necrosis is resorption of steapsin induced by 
pancreatic disturbances, although steapsin may be absorbed from 
the intestine. Some four or five cases have been observed in the 
dog, several cases in the sheep, and one horse was examined 
that was affected with fatty necrosis. In each of the above cases 



NECROSIS AND DEATH. 259 

there was evidence of pancreatic lesions, as inflammation, hem- 
orrhage and atrophy was noted in one case. Recently it has 
been suggested that this condition is caused by disturbances of 
the islands of Langerhan. 

The areas affected are at first soft and spongy, but later be- 
come more or less calcareous as a result of combination of lime 
salts with the free fatty acid. 

Fatty necrosis usually involves the omental fat, and espe- 
cially that in close proximity to the pancreas, though all fatty 
tissue is subject to this condition. 

In gross appearance the involved portions are dull, lusterless, 
opaque, slightly raised, usually circumscribed areas, of a yellow- 
ish white color. If the lesions are advanced, calcareous granules 
may be observed by palpation. In microscopic section the cells 
of the affected areas may contain needle-like crystals, or the cell 
substance may appear as a granular mass. 

3. Focal necrosis. — In certain infective diseases it has been 
noted that small foci of the various parenchymatous tissues un- 




%%%^0 1 «> 1 ««<«;si'%*>,«,%%«>,'%%vs i%%.a\^syHSi» 



Fig. 136. — A necrotic tubercle; lung-. x250. Showing- necrotic center surrounded 
by small round cells, cpitheloid cells, and leucocytes. 



260 VETERINARY PATHOLOGY. 

dergo necrosis. In many instances, this occurs in the absence of 
any circulatory disturbance, indicating that the exciting cause, 
chemic substance, is carried by the blood and appears to have 
a selective action for certain tissue. This t3^pe of necrosis is com- 
mon in diphtheria and typhoid fever in the human and in hog 
cholera, glanders, generalized tuberculosis and probably some 
other infective and chemically induced diseases of the lower ani- 
mals. 

The areas affected are frequently not sufficiently large to 
observe with the unaided eye. Microscopic sections show the 
cells in various stages of necrosis. The nucleus may be appar- 
ently normal or entirely disintegrated, the cell body may be 
granular or hyaline, it may be intact or appear fragmented. Leu- 
cocytic invasion of the necrotic area is of frequent occurrence, 
and may at first give the impression of an infected focus. Necro- 
tic tissue in focal necrosis may be absorbed and the destroyed 
tissue regenerated ; it may become liquefied, thus forming a cyst ; 
it may become infected and be succeeded by abscess formation, 
or it may be substituted with scar tissue. 

4. Jack-Sores. — This is a name applied to a very prevalent 
condition in jacks in which there is necrosis of the skin and sub- 
cutaneous tissue. Perhaps jack-sores should not be classed as 
a separate or distinct type of necrosis, but it is so common that 
it merits a special mention. The skin and subcutaneous struc- 
tures of the legs, venter surface of the abdomen and thorax, and 
maxillary region are most frequently affected. The necrotic 
areas may be very extensive, in some instances involving the 
entire metatarsal or metacarpal region. 

The etiology of "Jack-Sores" is not known, but no doubt it 
is the result of malnutrition and probably an irregular, indefinite 
lymphatic circulation is the prim.ary cause. 

Tissue Affected. — No tissue is exempt from necrosis. The 
tissue affected depends upon the cause, the animal and geog- 
raphical location. 

Disposition of Necrotic Tissue. — Necrotic tissue or products 
derived from it are more or less irritating and may produce an 
inflammation in the living tissue around the necrotic mass. 
The perinecrotic inflammation insures an increased number of 
leucocytes around and in the necrotic area. The necrotic tissue, 
leucocytes and other living cells may produce enzyms that 
will ultimately dissolve the necrotic tissue. There may be 
a contraction of the necrotic tissue and later it mav separate 
from the surrounding normal tissue. The reaction of the adja- 
cent living tissue may be limited and cause the production 



NECROSIS AND DEATH. 261 

around the necrotic area of a fibrous or osseous capsule, or even 
cause a fibrous formation throughout the entire necrotic mass. 
From the foregoing it is apparent that necrotic tissue may be 
disposed of as follows: 1. Absorption. 2. Exfoliation. 3. En- 
capsulation. 4. Sequestration. 

Absorption. — The necrotic mass is more readily absorbed 
when it is in a liquid state (coUiquation), although leucocytes, 
and various other cells may produce enzyms that are capable of 
dissolving coagulated necrotic tissue. Absorption of fluid ne- 
crotic tissue is in part accomplished by means of the lymphatic 
tissues, and in part by means of leucocytes that incorporate and 
convey fragments of necrotic cells to the various organs that 
dispose of waste materials. Necrotic infarcts are occasionally 
entirely absorbed. 

Exfoliation. — Necrotic surface tissue is frequently disposed 
of by separation of the dead from the living tissue as a result oi 
inflammation or contraction of the necrotic mass. The separated 
necrotic mass is the sphacelus. The process of separation and 
sloughing is exfoliation. Exfoliation is the usual disposition of 
necrotic extremities induced by freezing and by ergot poisoning. 

Encapsulation. — The irritation produced by subsurface ne- 
crotic tissue may be insufficient to cause an acute inflammation, 
but it may stimulate fibrous hyperplasia. Thus a fibrous capsule 
or wall is built around the necrotic mass, i. e., it becomes encap- 
sulated. In some instances the encapsulated necrotic tissue later 
becomes calcified, or it may become liquefied, the capsule retain- 
ing the liquid, thus a cyst is formed. 

Fibroblasts may extend into the necrotic area and form 
fibrous tissue throughout the entire mass, thus there would be 
a mass of cicatrizing fibrous tissue permeating the necrotic 
mass. 

Sequestration. — This is a term applied to the separation of 
subsurface necrotic tissue, more especially necrotic bone, from 
the surrounding healthy tissue. The separate necrotic portion 
is termed the sequestrum, and the process of its separation 
sequestration. An osseous sequestrum may be encapsulated, the 
capsule later becoming osseous, thus forming an involucre. 

Effects. — Necrosis is the condition resulting from tissue des- 
truction. The effects of tissue destruction depend upon the 
variety of tissue, the extent and location of the condition, and 
the age and condition of the animal in which it occurs. If the 
tissue destroved is capable of regeneration, or if it is limited in 
extent, and the animal is otherwise in good condition, the effects 
will be insignificant. If the tissue destroyed cannot be regener- 



262 VETERINARY PATHOLOGY. 

ated and is extensive, the animal will be deprived of that quan- 
tity of tissue and if the function of the destroyed tissue is of 
prime importance, the animal will die. 

N'ecrosis is invariably associated with inflammation, which is 
especially active around the necrotic area, and the results of 
this inflammatory reaction must also be considered in estimat- 
ing the sum total of the effects of necrosis. 



DEATH. 

DEFINITION. 
ETIOLOGY. 

Suspended heart action. 

Respiratory arrest. 

Suspended brain action. 
SIGNS. 

Post Mortem Staining. 

Temperature change. 

Muscular rigidity. 

Decomposition. 
TESTS. 

Mirror. 

Blister. 

Incision. 

Relaxation of sphincter muscles. 

Death is the condition resulting from the permanent arrest 
of all functions. Death should not be confused with necrosis. 
The former refers to somatic death and the latter to the death 
of a part. It is difficult and in fact impossible to determine the 
exact time when life ceases in a body. The various body tis- 
sues do not all become lifeless when the individual as a whole 
dies. The length of time that vitality is retained in the tissues 
of a dead animal depends upon the variety of tissue, the age of 
the animal and the cause of death. The less highly organized, 
the tissue, the longer its vitality is retained. The tissue of young 
animals possess their vitaliti^ for a longer time than the same 
tissues of an aged animal. Death results from disturbance of 
certain vital, centers and these tissues, as well as all others speci- 
fically acted upon by the agency that causes death, lose their 
vitality earlier than tissues not acted upon. 

Death may be physiologic or pathologic. 

Physiologic Death. 

This is that type of death observed in old animals. During em- 
bryonic life the principal function of all tissue cells is reproduc- 
tion. As the tissue becomes more matured, the reproductive prop- 
erty of its cells gradually diminishes and has practically disap- 



NECROSIS AND DEATH. 263 

peared in old age. Cell repair is complete in early life, but gradu- 
ally diminishes as the animal becomes aged. The activity of cells 
and their life cycle is limited as is that of all active structures 
either animate or inanimate. Therefore, if new cells are not pro- 
duced, and the old cells are not repaired their energy or vital 
forces are finally exhausted and they degenerate and die. If large 
numbers of cells of all tissues die the animal involved is incapaci- 
tated and ultimately sufficient cells die to diminish the function of 
the vital organs to such an extent that there is collapse and som- 
atic death. 

Physiologic death is initiated by a gradual decline which 
may continue until the individual dies. Or after a long per- 
iod of slow decline, death may be sudden as a result of a sudden- 
ly diminished function of a vital organ. Physiologic death is sim- 
ilar in a way to the collapse of the one horse chaise which, as the 
story runs, was used until it literally fell to pieces. Very few 
domestic animals die a physiologic death. Those animals whose 
flesh is used for food are butchered long before physiologic death 
would intervene, and those animals used as beasts of burden are 
usually destroyed when their earning capacity is monetarily less 
than the food they consume. 

Pathologic Death. 

Pathologic death signifies the ending of life prior to the time 
that the vital forces have been exhausted. 

Etiology. — Pathologic death is that type caused by accident 
or disease process. Death primarily is the result of permanent 
suspension of heart action, respiration or brain functioning. 

Suspended heart action may be caused by influences acting upon 
the cardiac nerve centers in the medulla or upon the heart mus- 
culature direct. The significance of suspended heart action is 
self evident. There being no blood circulating the tissue would 
soon consume all available nutriment and then succumb. Tem- 
porary arrest of heart action is called syncope. 

Respiratory arrest is usually the result of nervous influences 
though clonic spams of the respiratory muscles would produce 
a similar efifect. The absence of respiration implies the absence 
of oxygen to oxidize the blood and the tissues and the absence 
of oxygen for a considerable length of time results in carbon- 
dioxide poisoning and death. Apnoea is a condition in which 
respiration is arrested. 

Permanent arrest of all brain functioning even for a brief period 
results in cessation of all the principal functions and death. 



^64 VETERINARY PATHOLOGY. 

Thus, suspended brain function results in arrest of heart action 
and respiration either of which results in somatic death. Coma 
is a term used to designate a condition in which all conscious- 
ness or recognition of environments is suspended but the con- 
trol of vital functions is still maintained. 

Signs of death. — The changes that occur in dead tissue are 
of considerable importance especially to inspectors of carcasses 
of animals, the flesh of which is intended for human consump- 
tion. The most important post mortem changes in tissues are 
as follows; post mortem staining (livores mortis) ; death stiffen- 
ing (rigor mortis) ; and decomposition or putrefaction. 

Post Mortejn Staining. — The blood usually undergoes changes 
immediately after death. The disintegration of red blood cells 
allows of the liberation of hemoglobin which is deposited more 
or less extensively upon the inner lining of the blood vessels and 
heart and also filters through the vessels and stains the peri- 
vascular tissues. The length of time after death that post mor- 
tem staining becomes evident depends upon the cause of death. 
In fact the purplish staining along the cutaneous vessels evident 
in dead bodies may be evident in the living body of animals. Thus 
liberation of hemoglobin takes place during life in the blood of 
animals affected with septicemic diseases. 

Temperature changes. — The carcasses of all dead animals assume 
the temperature of the environment sooner or later. The length 
of time necessary for the body heat to pass out of a dead body 
depends largely upon the cause of death. In some diseases, 
those in which tissue change is limited, the temperature is sub- 
normal at the time of death and rapidly assumes the environmen- 
tal temperature after death. In other diseases, those in which 
tissue changes are extensive, the temperature may vary from 
normal to considerably above normal at the time of death and 
may increase for several hours after death. Temperature changes 
may be extremely variable in a carcass. Also a remarkably low 
subnormal temperature has been observed in many living ani- 
mals, especially those in a comatose state and yet the animals 
recover. The thermic variations should never be relied upon in 
determining whether or not life is extinct, at least not within 
48 hours after the animal is supposed to be dead. 

Rigor Mortis. — That the body of an animal becomes rigid after 
death is common knowledge to all observers. Rigor mortis re- 
presents a condition of the muscle fibre in which it becomes rigid 
as if in a tonic contraction. The length of time after death that 
rigor mortis appears and the length of time that it persists de- 
pends upon the condition of the animal at the time of death. 



NECROSIS AND DEATH. 265 

Thus muscular rigor appears usually in a few minutes after 
death and is of brief duration in animals, that have died as a 
result of a long continued exhaustive disease, as chronic tuber- 
culosis. On the other hand rigor mortis may not become evi- 
dent until 24 hours after death in animals that have been killed 
while in a perfect state of health and it may continue for from 
two to four days. In catalepsy, muscular rigidity is a charac- 
teristic symptom. Other conditions, however are sufficient to 
differentiate this from rigor mortis. 

Decomposition or putrefaction is caused by the action of putre- 
fying bacteria. 

The decomposition of a tissue is sufficient evidence of the fact 
that it is lifeless. Decomposition or putrefaction is not easily 
detected in the early stages. The evolved odor is usually the 
accepted sign of decomposition and during some seasons of the 
year, decomposition may not become evident for several days 
after death. The carcasses of animals dead of septic infections 
usually decompose immediately after death, e. g. carcasses dead 
of anthrax, hog cholera, etc. 

Tests. — Because of the uncertainty of the above signs espe- 
cially, during the first 24 or 48 hours after death, certain tests 
are recommended to determine the presence or absence of life 
in a certain body. They, like the above signs, are not absolute. 

The mirror test. — ^Respired air contains more or less water 
vapor. Respiration is not always perceptible. Water vapor is 
condensed upon a cold surface. The procedure of this test con- 
sists in holding a mirror over the nostril and if any air is ex- 
pired the watery vapor from the expired air will be condensed 
and rendered visible upon the surface of a mirror. This test is 
not infallible for the respiratory functions may be so diminished 
that the moisture (watery vapor) of the expired air is insufficient 
for condensation upon the mirror. 

Blister Test. — Blisters or vesicles can usually be produced by 
heat or chemic vesicants applied to the skin of a body in which 
life still exists. The formation of vesicles is not possible in dead 
tissue because the production of a blister represents the response 
of a living tissue to an irritant and only living tissues are cap- 
able of reacting. Vesicle productions varies in living animals 
and in some cases they are not produced. 

Incision. — Because of the elasticity of living tissues, all Incised 
wounds gap in the living body. Tissue elasticity disappears 
when the tissue dies, consequently incised wounds in dead tis- 
sues do not gap. 



2^ VETERINARY PATHOLOGY. 

Certain post mortem changes are rather constant in the eye. 
These changes consist of a cloudiness of the lens and the aque- 
ous humor, the condition gradually becoming more intense. 
The surface of the eye, i. e., the conjunctiva, becomes dry and 
scaly in appearance. 

All sphincter muscles are usually relaxed at the time of death 
and remain so permanently. 



CHAPTER X. 

TUMORS. 

(Neoplasms.) 

DEFINITION. 
FREQUENCY. 
STRUCTURE. 

Cells. 

Intercellular. 
Vessels. 
Nerve tissue. 
SIZE. 
SHAPE. 
COLOR. 

CONSISTENCY. 
NUMBER. 
GROWTH. 
EXTENSION. 
NATURAL RESISTANCE. 
RETROGRESSIJ'E CHANGES. 
CLINICAL CONSIDERATION. 
ETILOLOGY. 
VARIETIES. 
Occurrence. 
Primary. 
Secondary. 
Recurrent. 
Structure. 
Histoid. 
Organoid. 
Teratoid.. 
Clinically. 
Benign. 
Malign. 
Tissue. 
Adult. 

Epithelial and connective — Papilloma. 
Connective. 

Fibrous — Fibroma. 
Mucous — Myxoma. 
Cartilage — Chondroma. 
Osseous — Osteoma. 
Dentine — Odontoma. 
Adipose — Lipoma. 
Glia — Glioma. 
Muscular. 

Invo hint a ry — L eiomyom a. 
Voluntary — Rhabdomyoma. 
Vascular. 

Blood vessel — Hemangioma. 
Lymph vessel — Lymphangioma. 
Nervous. 

Neuroma. 



267 1 

\ 



268 VETERINARY PATHOLOGY. 

Embryonic. 

Connective. 
Sarcoma. 
Endothelioma. 
Hypernephroma. 
Placentoma. 
Epithelial. . ■ 

Carcinoma. 
Epithelioma. 
Adenoma. 
Hypernephroma. 
Plancentoma. 
Adult and Embryonic. 
Any and all tissues. 
Teratoma. 

The term "tumor" was formerly used to indicate any swelling 
in animal tissues. They, more than any other pathologic entity, 
have been studied and investigated by scientists, and yet little 
is known of their pathology. With the present limited knowledge 
it is impossible by definition to clearly differentiate them from 
some other pathologic conditions. They have been defined as 
new growths of tissue developing independently in any tissue 
of the animal body and atypical in structure and function. Also 
they are non-inflammatory growths of new tissue, persistent, 
independent of the surrounding structures, atypical in structure 
and function. A more concise idea can be formulated by think- 
ing of them as parasites, that is, they are new growths of tissue 
that develop in or upon the animal body at the expense of the 
animal, and are subject to the same pathologic conditions that 
the normal tissues are, as degeneration, necrosis, etc. 

Frequency. — Tumors are of frequent occurrence. They 
are more common in dogs particularly aged ones than in other 
animals. Of 127 animals presented in the daily clinic at tlie 
Kansas City Veterinary college during one college session, 12 
were affected with tum.ors. 

The frequency of tumors in animals treated in the Berlin, 
Dresden, and Munich veterinary colleges for an average period 
of seven years is shown by the following: 

Of 86,613 diseased horses, 1,113 suffered from tumors, or 1.3 per cent. 
Of 85,537 diseased dogs, 4,020 suffered from tumors, or 4.7 per cent. 
Of 4,972 diseased cattle, 102 suffered from tumors, or 2 per cent. 

Structure. — Tumors are composed of cells and usually, an 
intercellular substance. The cells ma), be similar to normal em- 
bryonic cells or to adult cells. The embryonic tumor cells differ 
from normal embryonic cells in that the former have no ten- 
dency to become matured while the latter have. The accom- 
panying cut shows a section of a sarcoma composed of embry- 



TUMORS. 269 

onic cells that are similar to embryonic connective-tissue cells. 
Papillomata are composed of cells that are very similar, if not 
identical, to adult epithelial cells, and are supported by an adult 
connective-tissue framework. 

Tumor cells are very similar to the cells of normal animal 
tissues. They have practically the same structure and require 
the same kind of nutriment. However, they do differ from the 
normal tissue cells in their power of growth and reproduction. 

Tumor cells are usually more susceptible to changed environ- 
ments than normal tissue cells. The nuclei of the cells of a rap- 
idly growing tumor are usually larger probably because of in- 
creased functional activity. 

The intercellular substance of tumors is as variable as the 
intercellular substance of normal tissues. Tumors having a 
mesodermal origin usually have an intercellular substance closely 
resembling that of normal connective tissue and hence may be 
mucus, fibrous, cartilaginous, or osseous. Tumors of an ectoder- 
mal or an entodermal origin may appropriate the pre-existing 
tissue framework for their stroma. Some tumors, like some 
normal tissues, are practically devoid of intercellular substance. 
Again, in some tumors the blood-vessels are the only intercellular 
substance. Anatomicallv the intercellular substance or stroma 
is an integral part of a tumor and its function corresponds to 
the function of intercellular substance of normal tissue. The 
cells and intercellular substance of tumors may be so arranged 
that the resulting structure approximates that of normal tissue 
(histoid tumors), but is never identical to a normal tissue. The 
different parts of a tumor may be assembled so that the resulting 
organization appears as an atypical gland or organ (organoid 
tumor), or tumors may be composed of structures derived 
from all three germ layers grouped indiscriminately but having 
some resemblance to an embryo (teratoid tumors.) 

Like normal tissue, tumors are usually nourished, by blood 
and lymph. The blood and lym.ph vessels may be structurally 
the same as normal vessels, or they may be composed entirely of 
tumor cells. The vessels have their origin from pre-existing ves- 
sels in the tissue from which the tumors are developed. They 
may be telangiectatic, cavernous, or plexiform, and their 
course is usually along the tumor stroma. Blood and lymph may 
also permeate the tumor through intercellular spaces, frequently 
resulting in hemorrhage or lymphorrhage. Some tumors have 
no blood or lymph supply, their nourishment probably being 
derived from consumption of normal tissue. 

Nerve cells and axones have been demonstrated in some 



270 



VETERINARY PATHOLOGY. 



tumors. They are, in some cases at least, a result of peripheral 
extension and development of the tumor tissue around normal 
nerve tissue, thus entangling it in the tumor. It is an open 
question whether nerve tissue exists in tumors except in those 
derived from normal nerve tissue or those in which normal 
nerve tissue is entangled. 

Leucocytes are common in tumors. Lymphocytes and poly- 
morphonuclear leucocytes have been demonstrated in the blood 
and lymph channels, perivascular and intercellular spaces, and 
within the tumor cells. The cells and the manner in which they 
are assembled, the structure and arrangement of the intercellu- 
lar substance, and the presence of the blood and lymph vessels 
indicate a common origin of tumor tissue and normal tissue. 




Fig. 137. — Section of Sarcoma, showing sarcomatous cells and blood vessels. 



Size. — Tumors are quite variable in size. They may become 
so large that they mechanically destroy life. An abdominal sub- 
serous lipoma, about the size of a wash-tub and weighing thirty- 
eight kilograms, (83i^ lbs.) was observed in an ox. A six- 
kilogram (13 ^/r, lbs.) fibroma was removed from the inferior 
cervical region of an eighteen kilogram (40 lbs.) dog. A twelve 



TUMORS. 271 

kilogram (26 2/5 lbs.) chondroma was obtained from the ster- 
num of a fifty kilogram (110 lbs.) sheep. All of the above tum- 
ors were of sufficient size to mechanically inconvenience the 
animals afflicted, and in one case resulted fatally. From the 
enormously large tumors there are all gradations to those 
miscroscopic in size, miliary tumors. The size of tumors is 
determined to some extent by the amount of nourishment sup- 
plied, the kind of tissue of which they are composed, and their 
location. 

Shape. — The form of tumors is largely determined by the loca- 
tion and the kind of tissue in which they occur. They may be 
spherical, ovoid, elliptoid, nodular, miliary, tubercular fungoid, 
polypoid, tabular, elongated cylindrical etc. Where there is no 
resistance or only a slight resistance there is a tendency to 
sphericity. In outline they may be regular or irregular, smooth, 
nodular or even granular and in some cases the exact outline 
cannot be determined. Large tumors that in shape approach a 
sphere are designated as spherical, ovoid, elliptoid, etc. Those 
that vary in size from a pigeon egg to a small pea are spoken 
of as nodular tumors. Miliary tumors are small spherical 
growths varying from a small pea to those microscopic in size. 
Spherical or oval tumors causing an elevation in the tissue in 
which they grow are known as tubercular tumors. Fungoid or 
projecting tumors are those that develop from the surface 
or sub-surface tissue, being attached to the normal tissue by a 
wide base. Polypoid tumors or polypi have the same origin and 
project as fungoid tumors, but are attached by means of a 
small pedicle. Tabular tumors are flat and usually develop be- 
neath the surface and especiallv beneath fasciae, tendons or liga- 
ments. . 

Color. — The color of tumors is dependent upon; first, the 
kind of tissue composing them ; second, pigmentation ; third, 
degeneration ; and fourth, the amount of blood they contain. A 
rhabdomyoma is more intensely colored than a fibroma, provided 
that the blood supply is the same in both, because of the hemo- 
globin in the muscular tissue. Melanomata and chloromata are 
so classified because of the deposition of pigment in them. Tum- 
ors, like normal tissues, become changed in color as a result of 
the various degenerations. Those having a limited blood supply 
are pale in color, while those having a large blood supply are 
highly colored. Hemorrhages may result in a deposition of 
hemoglobin or some of its derivatives, thus giving the tumor 
a mottled appearance. Mottling may also result from an un- 
equal blood supply. 



271 VETERINARY l^ATHOLOGY. 

Consistency. — Some tumors are soft and spongy, jelly-like, 
and from this type there are all variations up to those that 
are hard and resistant, bone-like. Their consistency is determined 
largely by the kind of tissue composing them and the secondary 
changes (degenerations) that affect them. Myxomata being 
largely composed of mucus are soft, fibromata are more resistant 
and osteomata are bone-like. Chondromata are usually quite firm 
and resistant, but they may undergo mudbid degeneration and 
become soft and spongy. Colloid degeneration is rather common 
in carcinomata, rendering them glue-like in consistency. Occa- 
sionally a tumor becomes calcified as a result of calcareous infil- 
tration. 

Number. — Tumors may be single, that is, a single one only 
occurring in the animal body. Single tumors are usually benign 
although they may be malign. An animal may be afflicted with 
a great many tumors at the same time (multiple tumors). Tum- 
ors may become multiple by metastasis. Tumors resulting from 
metastasis are designated secondary and the original tumor pri- 
mary. Multiple tumors may be malign, as sarcomata, carcino- 
mata, etc., or they may be benign, as multiple fibromata. Tum- 
ors that recur after they have been removed are designated recur- 
rent tumors. 

Growth. — The growth of tumors is the result of the inherent 
proliferative property of the tumor cells. Some tumors grow like 
an onion, there being a multiplication and accumulation of the 
central or internal cells, resulting in an interstitial expansion and 
an increase in the size of the tumor. Practically all benign tum- 
ors grow by interstitial expansion. Malign tumors grow by mul- 
tiplication of the peripheral cells and their infiltration as well as 
by interstitial expansion. The extent of growth of all tumors is 
proportional to the amount of nourishment they receive and to 
the adjacent tissue resistance. The relative amount of nourish- 
ment to tumor tissue and to normal tissue in the same body may 
be very unequal. Thus a tumor frequently receives an excessive 
amount of nourishment and grows rapidly, while the normal tis- 
sue in the same body is deprived of nourishment, resultmg in its 
atrophy or degeneration and emaciation. As a rule, the rate of 
growth is indefinite. Malign tumors grow more rapidly than be- 
nign. A tumor that is growing rapidly may cease growth, dim- 
inish in size, grow again and diminish again. Diminution in 
size may be succeeded by absorption and disappearance. 

Extension. — The manner of extension of the various tumors 
depends upon the migratory properties of the tumor cells and 
the relation and structure of the blood and lymph vessels. Tum- 



TUMORS. 



172> 



ors composed of embryonic cells extend more repidly than those 
composed of adult cells because embryonic cells are plastic and 
are to some extent capable of amoeboid movement. Adult cells 
are fixed in their form and none of them, excepting leucocytes 
and endothelial cells are migratory. The nutrient vessels of 
tumors are sometimes formed of tumor cells that are easily de- 
tachable, a structural peculiarity predisposing to tumor metas- 
tasis. 




Fig. 138. — Photograph of a section of a horse's lung, showing Metastatic Sarcomata. 



Benign tumors usually extend only by growth in continuity 
or contigufty. In fact, practically all tumors composed of adult 
tissues extend by pushing aside the normal tissue. Malign tum- 
ors are extended by blood, as sarcoma ; by lymph, as carcin- 
oma ; or they pass from one point to another through natural 
channels as the digestive and respiratory tracts. 

Summary. — Tumors may be extended ( 1 ) by growth in con- 
tinuity, (2) by growth in contiguity, (3) by blood, (4) by lymph, 
(5) by natural channels other than the blood and lymph vessels. 

Natural Resistance. — Normal tissues have a natural resist- 
ance to any injurious influence as the formation of tumors, in- 



274 VETERINARY PATHOLOGY. 

flammation, degeneration, etc. Tissue resistance to the devel- 
opment of neoplasms varies in different animals, in the same 
animal at different times, and possibly also in the different tis- 
sues of the same animal. The resistance of the surrounding 
tissue is made evident in some cases by the formation of a fibrous 
wall or capsule that limits and separates the tumor and the nor- 
mal tissue. Degeneration and necrosis may also be interpreted 
to be a result of opposed action by the invaded tissue. 

Retrogressive Changes. — ^Tumors are subject to the same 
degenerative processes that normal tissues are. Hemorrhages, 
necrosis and degenerations are frequent in tumors because 
of the imperfectly formed and irregular distribution of the 
supplying vessels. The results of hemorrhage into tumors 
depend upon the amount of extravasted blood and the secondary 
changes therein. A tumor the size of a cocoanut would likely 
become necrotic if a vessel ruptured and a half a liter of blood 
escaped into the tumor tissue. A small quantity of extravasate 
when infected with putrefactive microorganisms as a rule results 
in necrosis of the tumor tissue. Necrosis is a sequel of ob- 
structed circulation or results from the solvent action of meta- 
bolic products. Thus, necrosis may be the result of thrombosis 
or embolism. Thrombic formation is especially prevalent be- 
cause of the irregularities of the lining of the tumor vessels. 
Emboli are common, as they are frequently detached tumor cells. 
Circulation may also be interfered with by pressure of the tumor 
tissues, thus obstructing the efferent or afferent blood vessels. 
Some metabolic products of tumors constantly dissolve the sur- 
face cells, resulting in ulceration, a common necrotic condition 
observed in tumors. Tumors may be invaded with pyogenic 
bacteria, resulting in suppuration. 

Of the degenerations, mucoid and colloid are the most com- 
mon. Fatty degeneration and calcareous infiltration occur less 
frequently. Mucoid degeneration affects connective tissue and 
epithelial tissue tumors, occurring more frequently in the former. 
Colloid degeneration is found in epithelial tissue tumors. 

A four-kilogram (9-lb.) renal hypernephroma undergoing 
colloid degeneration was obtained on post-mortem examination 
of a three-year-old steer. Fatty degeneration usually succeeds 
necrosis in tumor tissue. Calcification of tumors is quite com- 
mon. Pigmentation is more common in tumors than in normal 
tissue. Melanomata are tumors containing melanin thg^t has 
been deposited in the tumor cells. Chloromata are tumors con- 
taining a green pigment. Hemoglobin, hematoidin and hemo- 



TUMORS. 



275 



siderin are frequently found in tumors after hemorrhage into the 
tumor tissue. 

Clinical Consideration. — Tumors are benign or malign. 
Benign tumors are usually encapsulated, i. e., they grow only 
by interstitial expansion ; are composed of adult or matured 
tissue ; have no tendency to recur when removed, and have only 
a mechanical effect upon the body in which they occur. Malign 
tumors are usually not encapsulated ; they grow by peripheral 
infiltration ; are usually composed of embryonic tissue ; fre- 
quently recur when removed, and have a tendency to kill by 
absorption of the metabolic products which are deleterious to 
the body. Malign tumors of domestic animals are not as fatal 
as they are in the human. Many horses affected with sarcomata 
have been permanently relieved by operation. 

Etiology. — There are some predisposing factors as heredity 
and breed peculiarities that are frequently involved in the devel- 
opment of tumors. Cadiot refers to a family of dogs in which 
the females were affected with carcinomata of the mammae for 







sy 3^ ir-jir * „4' 



-.aZ^£l ^CaJ^iiil 



,-^--r. ^,.t^--fj'. , :.,.^- 



Fig. 139.— Photograph of a horse affected with an ocular Epithelioma. 

This was a seaurl of a wire rut 



276 VETERINARY PATHOLOGY. 

two successive generations. Hereford cattle are more frequently 
affected with ocular tumors than any other breed. Injuries in 
which there is a destruction of the tissue surfaces predisposes 
to tumor formation, and, in many instances, in the human, sub- 
surface wounds are a causative factor in the production of 
epithelial embryonic tumors. A few cases of epitheliomata have 
been studied in the horse and ox that were secondary to injuries. 

The exciting causes of tumor formation have not been defin- 
itely determined, and this accounts for their undetermined char- 
acteristics. Many theories have been advanced. Cohnheim ad- 
vanced the idea that tumors were developed from misplaced 
embryonic cells (cell rests). This theory has received the sup- 
port of many pathologists. It is in accord with the general 
biologic law that every cell produces a cell like itself or ''like 
begets like." The supporters of this theory have not proved it, 
but the opponents have not disproved it. All biologists recog- 
nize the complexity of embryonic development and are aware 
of the possibility of cells becoming entangled or misplaced dur- 
ing the formation period. Experiments have demonstrated the 
possibility of successfully transplanting tissue, both embryonic 
and adult, into a foreign location in the body. Transplanted em- 
bryonic tissue, however, does not remain as such, but soon be- 
comes mature tissue, whereas malignant tumor cells have no 
tendency to become matured. Transplanted tissue cells do not 
infiltrate the surrounding tissue nor form metastases, but remain 
as distinct islands of cells. 

The parasitic theory has been supported by a large number 
of scientists. No doubt malignant tumors resemble infectious 
diseases in that they extend by metastasis and produce similar 
effects. However, the uncertain transmission of tumors from 
one animal to another is certainly antagonistic to the parasitic 
theory. 

Bashford, superintendent of the Imperial Cancer Research 
Fund, London, England, successfully transplanted 66 per cent 
of sporadic tumors. On the other hand, Ehrlich has successfully 
transplanted only about 14 per cent of sporadic tumors. No one 
has produced a satisfactory proof of the isolation of any causa- 
tive parasite. By some authorities bacteria were thought to be 
the active agent in tumor production, and by others protozoa 
were claimed as the causative factor, and, more recently, many 
radical observers have proclaimed that yeast were the cause. 
Some have even claimed that the tumor cells are parasites. 

Chemic disturbances, particularly changed chcmic reaction in 
a tissue, is responsible for tumor formation according to some. 



TUMORS. 



277 



An alkaline secretion at points where exposure and irritation 
occurs produces carcinomata (Hertzler). Following this thought 
an acid reaction in a normally alkaline tissue would tend to pro- 
duce sarcomatous tissue. 

The specific causative factor of tumor formation is not known, 
but it is something that excessively stimulates the reproductive 
power of cells. In fact, all other functions practically cease, the 
entire cell energy being expended in reproduction. That is,, 
tumors are the result of a disturbance in the cell metabolism in 
which reproduction is far in excess of the physiologic limit and 
is exercised at the expense of all other functions. 

Varieties. — There is no satisfactory method of classifying 
tumors. Some authors have attempted methods of classifying, 
but until more is known concerning them a classification is un- 
wise. The following is an attempt at grouping them, but is in 
no way complete. They may be grouped as to : 

OCCURRENCE. 

Primary — The original or Urst tumor. 

Secondary — Metastatic tumor. 

Recurrent — A newly developed tumor at the point from which 
one has been recently removed, 
STRUCTURE. 

Histoid — Simple tissue tumor. 

Organoid — Organ-like tumor. 

Teratoid — Mixture of various tissues resulting in a structure re- 
semhling an embryo. 
CLINICALLY. 

Benign — No tendency to kill. 

Malign — Having a tendency to kill. 

The following scheme shows the general structure and rela- 
tion of the various tumors: 



Adult Tissue 



Tumors- 



Connective 



Epithelium 



Muscular-myoma 



( Myxoma, Chondroma 
. \ Osteoma, odontoma, 
( Lipoma, Glioma . • • • 
Fibroma | p^p^j^^ 

fLeiomyoma 



loma 



\ Rhabdomyoma 



^T ^ • r Lymphangioma 

Vescular-angioma -^ tt • 

*= \ Hemangioma . . 

Nervous-neuroma 
Connective-sercoma 



( Round Cell ■ -^ 
\ Spindle Cell 



Embryonic Tissue^ 



\ Myeloid Cell 



y 



Placentoma 



Epithelium 



, Endothelioma , 

Carcinoma Hypernephoroma 

Adenoma | 

Epithelioma J 



J 



278 VETERINARY PATHOLOGY. 

FIBROMA. 

Fibromata are tumors composed of adult fibrous connective 
tissue. They occur in all animals. The skin and subcutaneous 
areolar tissue is their most frequent location, but no tissue is 
exempt. They are frequently found in the region of the sternum 
of the horse and ox, in the ovary and uterus of the cow, and in 
the perineal and elbow regions of the dog. In the skin and sub- 
cutaneous tissue they usually appear as loose, circumscribed, 
nodular growths. Some fibromata have no well defined border, 
or line of demarcation but are apparently diffused through the 
tissue. This type, however, is somewhat rare, and possibly they 
are not fibromata. Thev may become so large that their pres- 
sure produces atrophy, degeneration or necrosis of the skin cov- 
ering them, or the surface epithelium may produce sufficient 
new tissue to compensate for the increased surface. These tu- 
mors are usually single, that is, only one tumor occuring in the 
individual ; but they may be multiple. Multiple fibromatosis is 
occasionally observed in the subcutaneous tissue of horses. 
They are variable in size, being so small in many instances that 
they are not observed in an ordinary examination. A fibroma 
may be so large that the diagnostician would mistake it for a 
malignant tumor, a hernia, cold abscess, etc. Their shape is as 
variable as their size. They may be oval, tabular, tubercular, 
nodular, and, in fact, they may have any conceivable shape and 
contour. 

If the skin or coverinor tissue is incised or dissected awav the 
tumor is usually found to be surrounded by a fibrous capsule or, 
in rare instances, it may blend imperceptibly with the surround- 
ing normal tissue. They are not difficult to remove in their 
entirety because of their encapsulation. When they are excised 
their blood supply is found to be disproportionate to their size. 
With the small or limited blood supply there is a tendency to 
a slow growth and degeneration and necrosis. With an exces- 
sive blood supply there may be rapid growth and perhaps fre- 
quent hemorrhages into the tumor tissue. If the excised tumor 
is sectioned and the cut surface examined with the unaided eye, 
it appears to be composed of compact bundles of fibrous connec- 
tive tissue atypically arranged (hard fibroma) or of loosely ar- 
ranged bands of fibrous connective tissue inclosing areolar spaces 
(soft fibroma). In color the section appears pearly white with 
grayish-white, yellowish-white or dull pink areas, depending 
(Upon the compactness of the tissue, whether the fibre bundles 
are cut longitudinally or transversely, and the amount of blood 
contained. A fibroma is firm, dense and resistant, and when cut 



TUMORS. 



279 



into there may be a creaking sound similar to that produced in 
cutting a tendon. They have little or no tendency to peripheral 
infiltration but grow by central or interstitial expansion, mechan- 
ically pushing the contacting tissue aside. 

If the tumor has degenerated or become necrotic quite a dif- 
ferent picture than the above will be seen. It may be a mass of 
mucus as a result of mucoid degeneration. It may contain 
necrotic areas or the entire tumor may undergo necrosis, the 
necrotic tissue becoming liquified, coagulated, caseated or calci- 
fied. Hemorrhage into the tumor tissue may give it a mottled 
appearance. The hemorrhagic spots may be red, yellowish-red 
or greenish-red, depending upon the changes in th'e hemoglobin. 

Microscopically, the tumor tissue appears as white fibrous 
connective tissue, being composed of cells and a white fibrous 
intercellular substance. 




Fig-. 140. — Section of a hard Fibroma showing: 1. Transverse section of 
bundles of Fibres; 2. Longitudinal section of bundles. 



The cells are usually few in number, are flat and have a flat, 
oval nucleus. Cells are more prevalent in the rapidly growing 
tumors. The arrangement of the fibres varies and is the deter- 
mining factor of the denseness of the tumor. 

A hard fibroma is made up of bundles of fibres extending in 



280 



VETERINARY PATHOLOGY 



various directions and occupying practically the entire space, 
there being no interfunicular spaces. The bundles are compact 
masses of parallel, wavy fibres, with here and there a cell. The 
fibres are of two varieties, viz. : glia fibres and collagen fibres. 
Glia fibres are found along the surface of the cell and are parallel 
to its long axis. They are straight or slightly curved and prob- 
ably extend from one cell to another. Collagen fibres are out- 
side but lie close to the cell and appear slightly wavy. Collagen 
fibres predominate in fibromata. Blood vessels are few in num- 
ber and may be absent. 

A soft fibroma is composed of small bundles or bands of 
fibrous tissue loosely arranged. Cells and blood vessels are more 
numerous than in hard fibromata. The general appearance of a 
loose fibroma m.agnified one hundred diameters is very similar 




Pig 141. — Soft Fibroma, showing wavy loosely arranged fibres. 



to areolar tissue, except that in the former yellow elastic tissue 
is absent, while in the latter it is present. All variations in the 
compactness of the fibrous tissue is found from the soft to the 
hard fibroma. In fact some sections indicate that a soft fibroma 
becomes a hard fibroma by an increase in the intercellular fibres. 
Clinically, fibromata are innocent or benign tumors. Their 
rate of growth is relatively slow. They may cause a fatal termin- 
ation by mechanically obstructing the lumen of a hcllow organ, 
as the intestine, by pressure upon vital organs, as the brain, or 
they may become so large that the affected animal is unable to 
move about in search of its food. Thus Kitt mentions a fibroma 



TUMORS. 281 

that weighed 178 kilograms (391 Yg lbs.) They do not extend 
by metastasis, neither do they recur when removed. 

Fibromata can usually be differentiated from inflammatory 
new growths by the history of the case, fibromata having nu 
defined cause and inflammatory new growths resulting from irri- 
tation. Alicroscopically, inflammatory new growths contain mi- 
totic plasma cells and fixed connective tissue cells, while mitosis 
is rarely observed in fibromata. There is also an extensive blood 
supply in inflammatory growths, but a limited supply in fibroma- 
tous tissue. Actinomycotic and botryomycotic tissues are recog- 
nized by the presence of the causative fungi. Spindle-cell sar- 
comata may be confounded with fibromata and are sometimes 
difficult to diff'erentiate. Sarcoma cells usually contain more 
protoplasm than fibroma cells, and this may be used as a basis 
for differentiation. By a gross examination a leiomyoma may 
be mistaken for a fibroma, but the microscopic appearance of the 
nuclei is characteristic. The nuclei of fibroma cells are oval 
while those of leiomyoma cells are rod-shaped. If the fibroma 
contains degenerated or necrotic centers the differentiation may 
be more difficult in gross section but microscopic examination 
of the unchanged tumor tissue will be sufficient. When the en- 
tire tumor has degenerated or become necrotic diagnosis may 
be impossible. Fibromatous tissue may be found in other tu- 
mors or fibromata may become contaminated by permeation or 
infiltration of other tumor tissue as mucoid, sarcomatous, etc., 
resulting in a fibro-myxoma, fibro-sarcoma, etc. The first por- 
tion of the compound w^ord denoting that the mixed tumor con- 
tains more of that tumor tissue. Thus a fibro-myxoma is a 
tumor composed of fibroma tissue (fibrous connective) and myx- 
oma tissue (mucoid connective), the former predominating. 
Mixed tumors wall be discussed after consideration of the simple 
tumors. 

A keloid is a dense overgrowth of white fibrous connective 
tissues in a cicatrix. These growths are quite common in the 
negro, especially at the point of an injury, as a razor cut or ear 
puncture for an ear-ring, etc. Because of their frequency and 
extent they have been considered as tumors bv some authors. 
Thev are not true tumors but rather an inflammatory new 
growth resulting from improper cicatrization in wounds. They 
are not common in the lower animals. 



282 



VETERINARY PATHOLOGY. 



MYXOMA. 

Myxomata are tumors composed of mucoid connective tissue. 
These tumors may be a subvariety of fibroma. Purely myxo- 
matous tumors are not very common, occurring more frequently 
in combination with other tumor tissue. They are usually found 
in connective tissue, but in no special location. They have been 
found in the heart, along nerve trunks, in the nostril, and a case 
has been reported of a pure myxoma involving the entire orbital 
structures in a horse. These tumors are usually about the size 
of a hen's egg, rarely becoming very large, probably because of 
their destruction by degeneration. They are invariably single. 
They appear as semi-solid masses, surrounded by fibrous cap- 
sules and are usually dirty-white or gray in color. After they 
are removed and an incision made into them a mucus or gela- 
tinous, ropy fluid escapes. The cut section appears as a glassy, 
semi-transparent, semi-solid mass and is very similar to Whar- 
ton's jelly. The escaped fluid will be found by chemical test to 
contain considerable mucin. Their blood supply is usually very 
meager, in fact some authors regard myxomata as a mucoid 
degeneration because of their limited blood supply. 

Microscopically, a myxoma is composed of stellate cells, in 



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Fig. 142. — Section of Myxoma from the orbital fossa of a hoi'se, 
showing stellate cells. 



TUMORS. 283 

v/hich the cell processes are apparently continuous with the pro- 
cesses of adjacent cells. Myxoma cells have an oval nucleus and 
the spaces between the cells and cell processes are filled with 
mucus, which appears as a stringy, gray substances that stains 
red with eosin. Myxomatous cells produce both kinds of fibres, 
i. e., glia and collagen fibres. Tl^e collagen fibres are more or 
less separated from each other by a varying quantity of fluid 
containing mucin. Myxomata are prone to degeneration, result- 
ing in the formation of a cyst, or the fibrous capsule may become 
eroded, allowing the degenerated contents to escape into the sur- 
rounding tissue or upon a surface. In the latter case the degen- 
erated contents is usually absorbed. Cicatricial tissue is usually 
produced in the cavity or space occupied by the myxoma. Sub- 
surface, myxomatous, degenerated areas may become infected, 
resulting in abscess formation. 

Clinically, myxomata are benign tumors. They grow slowly 
by interstitial expansion, do not recur when removed, and ex- 
tend only by continuity or contiguity. 

These tumors are dififerentiated from mucoid degeneration, as 
the latter contains no stellate cells, and there are usually some 
of the cells present in mucoid degeneration that are normally 
present in that area. Clinically, it may at times be difficult to 
distinguish between mucus retention cysts and myxoma, but by 
the exploring needle the contents of the cyst may be evacuated 
and thus the nature of the mass will be determined. 

CHONDROMi^ 

A chondroma is a cartilaginous tumor. They occur in cattle, 
sheep, dogs, horses and fowls. They are found most frequently 
in the location in which cartilage is normally found. The ster- 
num seems to be a favorite location for their development, prob- 
ably because of the frequent injuries of the sternal cartilage due 
to the fracture of ribs and other injuries. They not infrequently 
occur in other bones, possibly developing from islands of cartil- 
age that have not ossified, or from marrow or periosteum. They 
also occur in glandular tissue as the thyroid, parotid, ovary and 
testicle, and a few cases of chondromata of the lung have been 
reported. 

These tumors appear as hard, nodular, well-defined growths, 
unless they are undergoing degeneration. In this case they may 
be of the nature of cysts, or if their capsule is ruptured, they may 
be soft, spongy, dififuse masses. They are variable in size. A 
chondroma weighing 12 kilograms (26 1/5 lbs.) was obtained 



284 



VETERINARY PATHOLOGY. 



from the sternum of a sheep killed in a Kansas City abattoir. 
Another about the size of a pigeon's tgg and attached to the 
sternum of a small hen was found by a city meat inspector. 

Their shape is very irregular, but they are most frequently 
oval. As a rule they have a regular surface, though they may 
be lobulated. They are usually separated from the surrounding 
tissue by a fibrous capsule, but they may be firmly adherent to 
the adjacent tissue. In cutting, the tumor gives a resistance sim- 
ilar to cartilage and they may be gritty because of calcification 
or ossification. The ablated tumor is bluish-white if it is a pure 
chondroma. Degenerated areas will vary in color according to 
the kind and degree of the degeneration. Necrotic centres appear 
dull gray or yellowish-white and white if calcified. If the tumor 
is mixed the color will vary according to the contaminating tumor 
tissue. 

Chondromatous tissue is composed of cartilage cells and an 
intercellular substance. The cells are irregular in size and shape 
and the number found in each lacuna is more variable than that 
in normal cartilage. The size, shape and arrangement of cells in 
different areas in the same tumor is variable. The cells are fre- 
quently degenerated, the nucleus fragmented and the cell mem- 
brane ruptured, allowing the cells to fuse as a homogeneous 



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Fig. 143. — Section of Chondroma from sternum of a sheep, 
showing lacunae with inclosed cartilage cells. 



TUMORS. 285 

mass. The lacunae are not so distinct as those in normal cartil- 
age, and their capsule may be absent. The intercellular substance 
is usually homogeneous, as in normal hyaline cartilage, or it may 
be fibrous, as in normal fibro-cartilage or elastic cartilage. The in- 
tercellular substance becomes fibrous towards the margin of 
the growth and finally forms a perichondrium. The cells may be 
arranged in rows near the perichondrium, but they are more 
likely to be irregularly distributed. The microscopic appearance 
of a degenerating, necrotic or mixed chondroma depends upon 
the kind and extent of the condition existing. 

Clinically, chondromata are usually benign, but they may be- 
come malignant because of their extent. Some surgeons have 
recorded esses of metastatic chondromata. These tumors are 
frequently lobulated and may be multiple. They have little ten- 
dency to recur when removed. 

LIPOMA. ! 

Lipomata are tumors composed of adipose tissue with a con- 
nective tissue framework supporting the vascular supply. They 
occur quite commonly in the horse, ox, and dog, but none of the 
domestic animals are exempt. They usually develop where adi- 
pose tissue normally exists, as the subcutaneous tissue, submu- 
cosa and subserosa, omentum, etc. They may also occur in tissue 
that contains no fat, as the liver, kidnc}^ and even the brain. 
They occur most frequently in the subcutaneous tissue in the 
horse ; in the intestinal and omental subserosa of the ox and 
hog; in the subcutaneous and conjunctival submucosa in the 
dog, and in the uterine submucosa of the sheep and the cow. 

Lipomata are usually circumscribed, but thev may be diffuse. 
The accompanying cut is from a photograph of a two-year-old 
colt in which there is shown a diffuse subcutaneous lipoma of 
the left hind leg. These tumors mav become enormous in size 
in the horse and ox, some cases having been reported of lipomata 
as large as a wash-tub and weighing 30 to 70 kilograms (66 to 
154 lbs.). In consistency, these tumors mav be firm and dense 
or soft and flabby. They are usuallv surrounded by a fibrous 
capsule and in section those from the peritoneum and omentum 
ere yellowish or white in color. Peritoneal, omental, submucous 
and subcutaneous lipomata have a smooth surface ; intestinal 
lipomata are usually lobulated. Bands of connective tissue may 
divide the tumors into lobes or lobules or the connective tissue 
may be diffuse throughout the entire structure. In cutting a 
lipoma the resistance varies according to the quantity of fibrous 
connective tissue it contains. If osmic acid is applied to the free 



286 



VETERINARY PATHOLOGY. 



surface of the gross specimen it stains the adipose areas black 
but has no effect upon other tissue. Occasionally groups of adi- 
pose cells become necrotic and calcify, thus forming gritty areas. 
Complete necrosis with sloughing or calcification is not rare in 
the larger lipomata. 




Pig. 144.- — From photograph taken 6-20-*7 of a colt affected with a 
Liipoma. Photograph presented by J. IT. arcNeil. 



Subcutaneous 



TUMORS. 



287 



Microscopic sections of lipomatous tissue closely resemble 
normal adipose tissue, except that the cells may be larger and 
perhaps more irregular in shape. As in normal adipose tissue 
the adipose cells are supported by connective tissue cells and 
fibres. The application of Sudan III and osmic acid gives 
further proof of the composition of the cells. 

Lipomata may be multiple but they are typical benign tumors, 
though death may result from the mechanical effects produced 




Xfo 



Fig. 145. — Section of 



a Lipoma from omentum of an ox, showing framework, 
of adipose cells. 



by them. They do not form metastases. Subserous lipomata pro- 
duce volvuli which terminate fatally in horses. Large periton- 
eal or omental lipomata of the ox and dog frequently cause suffi- 
cient displacement of the abdominal organs to materially de- 
range their function. Subcutaneous carpal lipomata in the horse 
may become so large that they mechanically interfere with loco- 
motion. Lipomata may have a fibrinous infiltration and organ- 
ization resulting in lipomatous elephantiasis. 



288 VETERINARY PATHOLOGY. 

OSTEOMA. 

An osteoma is a tumor composed of osseous tissue. Pure 
osteomata are not commonj They occur most frequently in re- 
lation to bones and usually at the union of osseous tissue devel- 
oped from different ossifying centres. These tumors are quite 
common in mules, appearing as projecting pedunculated masses 
attached to the inferior maxilla. More rarely they are found in 
other organs, as the lung, parotid gland, mammary gland, etc. 






Fig. 146. — Perdunculated Osseous Tumor Maxilla. Horse. 

These tumors are usually small, rarely becoming as large as 
a cocoanut. They are hard, nodular masses that are frequently 
lobulated and usually firmly attached to the surrounding tissue. 
It is possible that they are developed from osseous cells which 
have been misplaced in bone formation or from the osteogenetic 
layer of the periosteum. When they develop adjacent to pre- 
existing bone the periosteum or endosteum surrounds them. 
Those osteomata developing in other structure than bone are 
surrounded by a distinct membrane which is usuall}^ very sim- 
ilar to periosteum. Osteomata may be classified as: (1) hard, 
ivory or eburnated, and (2) soft, spongy or cancellated. Either 
of the foregoing classes may be homologous or heterologous. 
Homologous osteomata occur in bonv structures and may be an 
exostosis or an enostosis. Heterologous osteomata occur in other 
tissue than bone. 

Hard, ivory or eburnated osteomata are structurally very 
similar to the compact osseous tissue of a long bone. Haversian 
systems may be present or they may be absent. If the Haversian 
systems are present they are irregularly arranged and are ap- 
proximately perpendicular to the surface of the related bone. If 



TUMORS. 289 

the Haversian systems are absent the tumor is composed of 
superimposed lamellae like the outer circumferential lamellae of 
the shaft of a long bone. 

Soft, spongy or cancellous osteomata are surrounded by a 
periostoid membrane. In structure they are similar to cancellous 
osseous tissue. The marrow spaces may be occupied by tissue 
that is structurally identical to red marrow or they may be filled 
with sarcomatous tissue, fibrous connective tisssue, etc. The 
blood vessels are usually normal in structure and their distribu- 
tion is through Haversian canals in the hard osteoma or the 
spaces in the soft osteoma. 

Osteomata are invariably single; do not recur when removed; 
have no tendency to form metastases ; and hence are benign. 

They should be diiTerentiated from (1) ossification of inflam- 
matory new growths as ringbone, spavin, myositis ossificans, 
etc. ; (3) hyperplasia of osseous tissue ; (3) ossification of tumor 
tissue as fibromata, chondromata, etc. ; (4) metaplasia in which 
osseous tissue is the end product; (5) calcification. 

GLIOMA. 

A glioma is a tumor composed of supporting cells (neuroglia 
cells) of the tissue of the central nervous system. Neuroglia 
tissue occurs in two forms, as ependymal cells lining the neural 
canal and the ventricles and as glia cells which are derived from 
the ependymal cells and act as a supporting framework of the 
central nervous system. Gliomata are of two types, depending 
upon the type of cells composing them, viz., spider cell glioma 
and mossy cell glioma. Gliomata have been observed only two or 
three times in the domestic animals. They usually have their 
origin in the gray matter near the central canal of the spinal : 
cord or in the gray matter of the cerebrum. They do not become ? 
large and they are usually not encapsulated. They are composed 
of cells that are very similar to normal neuroglia cells. The ■ 
glioma cells mav be slightty larger than neuroglia cells but they 
have the fibre-like processes characteristic of them. 

These tumors do not form metastases but are likely to produce 
a fatal termination by pressure upon nerve centers. 

ODONTOMA. 

Odontomata are tumors composed of dental tissue and usu- 
ally occur in connection with teeth, particularly the superior 
molars. Odontomata are Of frequent occurrence, the majority 
of dental diseases in two to five-year-old horses being due to 



290 



VETERINARY PATHOLOGY. 



them (Williams). Facial bulging is a common symptom of 
them and there may be an excessive mucus discharge from the 
nostrils. Cystic odontomata may produce super-resonance, which 
is useful in differentiating them from empyema of the facial 
sinuses. 

These tumors are derived from the enamel organ, dentine 
papilla, or the tooth follicle. Their derivation to some extent 
determines their structure. Those derived from the enamel 
organ are composed of an enam.el covering and in some cases 
the entire odontoma is enamel. Dentine is usually the pre- 
dominating tissue in those derived from the dentine papilla. 
From the tooth follicle there are usually formed cystic odonto- 
mata, although they may be fibrous or may contain ossified cen- 
tres and cementum. Their structure varies considerably and it is 
not rare that all of the above structures are represented in one 
odontoma. 

In size, odontomata vary from microscopic masses to irregu- 




Fig. 147. — Photograph of an Odontoma of the interior maxilla of a horse. 



TUMORS. 291 

lar bodies. Their shape and color are as variable as their size. 
Epithelial or enamel odontomata are the highest in the scale of 
hardness of all tumors. Other types of odontomata are soft. 
Cystic odontomata may be single or multiple, as many as three 
hundred having been observed in a single follicular tumor of 
this type. They may grow very rapidly but more frequently 
they develop slowly. They have no tendency to form metastases. 
Degeneration is common in those developing from the tooth 
follicle. Clinically they are benign but may cause fatal termina- 
tion mechanically or from infection. 

According to the derivation Sutton describes four classes of 
odontomata as follows : 

1. Those derived from the enamel organ or epithelial odonto- 
mata. They usually appear as irregular masses covered with 
enamel. They may contain cystic cavities separated by enamel 
partitions. Epithelial odontomata are usually surrounded by a 
firm capsule, and in some instances appear to have had their 
origin from a mucous membrane. Miscroscopically they are found 
to be composed of enamel cells and irregular columns of epithe- 
lial cells forming alveoli. The epithelial cells vary in shape from 
columnar to the stellate or typical progenitors of enamel. These 
tumors occur in most of the domestic animals and usually in 
early life. Two epithelial odontomata were ^obtained from the 
left maxillary sinus of an aged horse used for dissecting pur- 
poses. These odontomata were completely enclosed in an osse- 
ous mass, the maxillary sinus being completely filled bv the new 
growth. The facial bones were slightly bulged. The osseous 
formation surrounding the odontomata and the thickening of the 
facial bones indicated that considerable time had elapsed since 
their formation. 

2. Those derived from the tooth follicle. Depending upon the 
nature of the neoplasm this group may be further subdivided 
into follicular and fibrous odontomata, cementomata and com- 
pound follicular odontomata. 

Follicular odontomata result from hyperplasia of the tooth 
follicle tissues which thus prevents the normal eruption of the 
tooth. They may appear as simple or multiple cysts. Their 
walls may be calcareous or osseous but they are more frequently 
membranous. The cysts are usually subdivided into many com- 
partments, the cavities of which are lined with epithelium. This 
lining epithelium secretes a viscid fluid, the accumulation of 
which is responsible for the enlargement of the cysts. They 
occur in sheep, hogs and horses. 

Fibrous odontomata are produced by a marked increase of 



192 



VETERINARY PATHOLOGY. 



the enveloj)ing fibrous capsule of the follicle. The hyperplastic 
fibrous tissue usually fuses with the cementum, and the entire 
mass may later become calcified or ossified. These odontomata 
are most common in ruminants, goats especially being affected. 
They are prone to occur in animals afiiicted with rickets. 

Cementomata (Osteocystoma capsulare dentiferum) are 
formed by ossification of excess tissue developed around the 
tooth follicle. The hyperplastic cementum may include several 
tooth germs. They appear as masses of cancellous or spongy 
bone and are structurally very similar to cementum, being com- 
posed of irregular spaces surrounded by osseous tissue contain- 
ing branched lacunae. They are most comm.on in horses, occur- 
ing most frequently in connection with the incisor teeth. 




Fig. 148. — Epithelial Odontoma. 



Compound follicular odontomata result from the ossification 
of irregularly located areas of the tooth follicle tissues, thus 
leaving intervening areas of fibrous tissue. The ossified masses 
are designated denticles and they may be very numerous, as 
many as three hundred having been observed in a single tumor. 
The intervening tissue usually degenerates and becomes of a 
liquid consistency. Thus the tumor appears as a cyst containing 
many cavities. The denticles vary in size and consistency. These 
tumors have been observed in the goat, sheep, ox, and horse. 



TUMORS. 



293 



3. Radicular odontomata are those derived from the dental 
papilla, developing from the roots of a tooth after the crown 
has formed. They appear as bony masses and are frequently 
enclosed within the m.axilla. Structurally, they consist of den- 
tine and cementum, the dentine usually being surrounded by a 
cemental capsule. They are occasionally observed in domestic 
animals, being most common in boars. 

4. Composite odontomata are composed of varying amounts 
of irregularly arranged enamel, dentine and cementum. A single 
tumor may contain several teeth fused into one mass. Their 
structure varies with the amount of each of the above named 
constituents they contain. Thus they may be almost entirely 
enamel or contain a very little enamel. They may be solid and 
massive or cystic. They are very likely to cause suppuration 
and necrosis of the adjacent tissues. This type of odontomes 
occurs more frequently in the horse. 

Dentigerous cysts are more properly classified as a type of 
teratomata and will be discussed with that group of tumors. 

NEUROMA. 

Neuromata are tumors composed of nerve tissue. They are 
exceedingly rare. They occur in connection with ganglionic 
cells and most frequently those of the sympathetic ganglia, al- 
though they may occur in the brain. They appear as nodular 
growths varying from the size of a pin head to that of an apple 
They are gray or white in color, rather firm, and usually sur- 
rounded by a capsule. Irregularly shaped ganglionic cells inter- 
posed with some nerve fibres constitute their minute structure. 

These tumors should be differentiated first from the so-called 
"amputation neuromata," which are simply an entangled mass 
of regenerated axones and are not tumors ; second from fibromata 
that develop from the perineurium or endoneurium of a nerve 
trunk. 

Neuromata may be multiple but they are benign. 

ANGIOMA. 

These are vessel tumors that are developed independently of 
pre-existing vessels. But it is frequently impossible to deter- 
mine whether the mass of vessels is a result of excessive growth 
of the pre-existing vessels (hyperplasia) or whether they are 
newly-formed vessels. 

Possibly angiomata should be discussed under the caption of 



294 



VETERINARY PATHOLOGY. 



endotheliomata as it has been thought by some that the endothe- 
lium is the only neoplastic portion of an angioma. 

This group is composed of (1) hemangiomata. (2) lymphan- 
giomata. * 

Hemangiomata are blood-vessel tumors. In the human they 
are found most frequently in the skin and may occur in the skin 
in domestic animals, but are not often observed there because 
of the pigmentation of the skin. They are found most frequently 
in the liver and the spleen of the ox, dog, horse and sheep. An 
occasional case is observed in the subcutaneous tissue of the 
horse. Hemangiomata may be subdivided into four varieties. 

Hemangioma simplex (Capillary telangiectases, nevus, birth 
mark) is a tumor in which there is an excess of capillary vessels 
are considerably enlarged or dilated. The vessel wall is usu- 
ally altered in structure, the endothelial cells being larger and 
the perivascular tissue more dense. These are quite common 
in the liver of the ox where they appear as irregular blood spots, 
red or purplish in color. 




Fig. 149. — Haemangfioma Simplex. 

a. Large capillaries engorged with blood. 



b. Liver cells. 



Cavernous hemangioma (hemangioma cavernosum) is a tumor 
composed of spongy tissue similar to erectile tissue. The caver- 
nous spaces are filled with blood, thus coloring the tumor red or 
bluish-red. These tumors are found most frequently in the liver 
and spleen. An ox liver containing cavernous spaces, each as 
large as a hen's egg and containing parietal thrombi, has been 
observed. A lobulated enlargement in the spleen of a dog was 



TUMORS. 



295 



found to be a cavernous hemangioma. The spaces in cavernous 
hemangiomata are lined by endothelium that is supported by a 
very limited amount of white fibrous connective tissue, yellow 
elastic tissue being practically absent. 




Fij,-. 150. — Photograph of spleen of dog affected with an Hemangrioma Carvernosum. 



Heinavogioma hypertrophicum is a blood-vessel tumor composed 
of masses of relatively small vessels, in which the vessel walls 
are hypertrophied. One of these tumors occurring in the subcu- 
taneous tissue of the metacarpal region of a horse has been 
observed. It appeared as a mass beneath the skin and was 
about the size of a hen's egg. Pulsations could be observed and 
by palpation they w^ere quite distinct. The tumor when removed 
was a tangled mass of blood-vessels with comparatively small 
openings. Microscopically, the vessel walls were found to be 
hypertrophied. The vessels were held together by fibrous con- 
nective tissue. 

Cirsoid aneurisms are tumors composed of dilated and enlarged 



296 



VETERINARY PATHOLOGY. 



tortuous arteries. This variety of hemangiomata is not common 
in the domestic animals. 

Lymphangiomata are tumors composed of newly-formed lym- 
phatic vessels. These tumors are not common ; in fact, only one 











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Fig. 151. — Section of Hemangnloina Hypertrophicum, showing- an increase in 
the number of the vessels and an hypertrophy of their walls. 

or two cases have been reported by veterinarians. The tumors 
may be conveniently divided into capillary and cavernous. 

Angiomata are usually benign tumors, although by rupture 
they may produce fatal hemorrhage or lymphorrhage. 



MYOMA. 



Myomata are muscle tumors. They are divided into two 
classes : 1. Leiomyomata or the smooth muscle tumors. 2. 
Rhabdomyomata or the striated voluntary muscle tumors. My- 
omata, found occasionally in the human, are rare in the lower 
animals. 



TUMORS. 



297 



Leiomyomata are found most frequently in those locations in 
which involuntary muscle tissue normally exists, as the uterus, 
bladder, intestine, etc. They are nodular or diffuse, dense, pale 
pink masses appearing very similar to fibromata. Microscopic- 
ally they are composed of miscellaneously arranged involuntary 
muscle cells. They differ from fibromata in that the muscle cells 
are thicker and usually not as long as the fibres of fibromata. 
Frequently they are combined with fibromata forming a leiomyo- 
fibroma, making the diagnosis more difficult. Leiomyoma cells 
may be very similar to the cells of a spindle-celled sarcoma, but 




Fig. 152. — Leiomyoma, small intestine, mule. 



the nuclei of the former are long and rod-shaped while those 
of the latter are oval in shape, a characteristic usually sufficient 
for diagnosis. The cytoplasm of .the leiomyoma cells stains 
densely with acid stains. 

Rhabodomyomata have been found in the kidney, ovary and 
testicle. They are probably the result of the development of 
misplaced embryonic myoblasts. These tumors are usually pale 
in color. In microscopic section the cells are irregularly striated, 



298 



VETERINARY PATHOLOGY. 



and are variable in shape and arrangement. These tumors are 
benign. 




Fig. 153. — Leiomyoma. 

a. Smooth nucleus cell, showing nucleus. 



SARCOMA. 



A sarcoma is a tumor composed of embryonic connective tis- 
sue cells. The cells have no tendency to become mature but 
constantly appear as undifferentiated embryonic cells. Sarcomata 
are of frequent occurrence in all domestic animals. They have no 
predilection for tissue or location, and are variable in size and 
shape. They may be circumscribed but are more frequently dif- 



TUMORS. 



299 



fuse. Metastases are frequent in the lungs, liver and kidney. 
Metastatic sarcomata are usually circumscribed. 

Sub-surface sarcomata may produce necrosis of the surface 
tissue, the tumor projecting as a red, granular mass, which ap- 
pears very similar to exuberant granulation. The surface tissue 
may not be destroyed, the tumor appearing as a sub-surface 
nodule or diffuse mass. Some sarcomata are encapsulated and 
are easily enucleated, but the malignant varieties have no cap- 
sule and it is impossible to differentiate the surrounding tissue 
from that of the tumor. Sarcomatous tissue may be soft and 
spongy or hard and dense, depending upon the extent of the 
mtercellular substance and the kind of cells composing it. In 
color they vary from gray or white to pink and they may be 
mottled, depending upon hemorrhage, pigmentation, or necrosis. 

The microscopic appearance varies with the different varie- 
ties, but in general they are composed of embryonic cells having 




Fig'. 154. — Photograph of a horse affected with Sarcoma of the Mediastin'uiti result- 
ing' in obstructed circulation. 
(a) Oedema inferior thoracic regrion. (c) Subcutaneous veins, 

(to) 3u^ Itr vein engorged with blood. 



300 



VETERINARY PATHOLOGY. 



a limited amount of intercellular substance. The cells may be 
round, spindle, or myeloid, and the intercellular substance may 
be mucoid, fibrous, cartilaginous or osseous. The cells contain 
a large centrally located ovoid nucleus, occupying practically 
the entire cell body. Mitotic figures are common in rapidly 
growing sarcomata. Frequently there are multipolar mitotic 
figures indicating the possible division of a cell into three or 
more daughter cells. Karyolysis or nuclear fragmentation is 
well marked in those cells that are centrally located in the tumor, 
that, is, in degenerating centres, and in cells of sarcomata that 




Figr. 155. — Section of tumor, showing mottled appearance, a result of Necrotic centres 



TUMORS. 



:3i 



are not growing rapidly. The portion of the cell body not occu- 
pied by the nucleus is composed of undifferentiated protoplasm. 
In appearance the intercellular substance varies according to 
its composition. An abundance of capillaries and small blood 
vessels are found in sarcomata. These may be normal in struc- 
ture or they may be infiltrated with sarcomatous tissue, and, 
in some cases, the blood flows through channels formed by sar- 
coma cells. Hemorrhage is of frequent occurrence in sarcomata. 
The blood vessels have no regularity in their distribution, a 
structural peculiarity frequently resulting in degeneration and 
necrosis. Lymphatic spaces and vessels are absent in sarcomata, 
excepting lympho-sarcomata, unless they are entangled during 
the development of the tumor. Nervous tissue has not been 
demonstrated as a distinct entity in sarcomata. There are usu- 
ally many leucocytes and frequently some plasma cells in sar- 
comatous tissue. The plasma cells may produce the intercellular 
structures of sarcomata or they may become adult connective 
cells and produce fibrous connective tissue. 




Fig. 156. — Round cell Sarcoma. 



The rapid development and the irregular distribution of blood 
vessels predispose sarcomata to destructive processes. Mucoid 
degeneration frequently occurs and may result in the complete 
destruction of the tumor. Necrosis is also quite common, and 
suppurative conditions are not rare. If the normal tissues are 
eroded, exposing the tumor tissue, septic infection is common 
and sometimes results fatally. 

This group of tumors may be classified, according to their 



302 



VETERINARY PATHOLOGYo 



cellular elements, as (1) round-celled sarcomata, (2) spindle- 
celled sarcon.^ata, and (3) myeloid-celled sarcomata. 

Round-cell sarcoma. This tumor is composed primarily of 
round cells (spherical cells) and is rather common. They de- 
velop in any tissue and are, as a rule, the most malignant tu- 
mors of this entire group. They are soft, spongy, and usually 
quite vascular, and, as a rule, are not encapsulated. 

Structurally the cells of this variety approximate the embry- 
onic epithelial cells more closely than do those of any of the 
other types. According to the size of the cells two classes may 
be recognized, viz. : small and large. There is, however, no dis- 
tinct line between the two classes. The small, round cells are 
about the size of lymphocytes while the large, round cells are 
as large and sometimes much larger than mononuclear leuco- 
cytes. The nuclei of this type of sarcoma cells are, relatively, 
much larger than the nuclei of lymphocytes or leucocytes. In 
fact, the nucleus occupies practically the entire cell body. The 
intercellular substance is very limited and is usually mucoid or 
reticular. Blood vessels are usually numerous, and their walls 
are frequently formed by sarcomatous cells. Metastatic growths 
are frequently in this type. The cut on page 273 is from a pho- 
tograph of the lung of a horse, showing metastatic round-celled 




Fig. 158. — Photograph of sheep's heart, showing a lympho sarcoma of the 

pericardium. 



TUMORS. 



303 




Fig. 158. — Section of a Lympho Sarcoma of a dog's omentum, showing the 
lymph vessels and sarcomatous tissue. 



sarcomata. The primary tumor involved the eye-ball and finally 
destroyed the soft structures of the entire orbit. In this case 
two or three metastatic tumors were observed in the liver also. 
The cut on page 299 is a photograph of a horse in 
which there was an extensive sarcomatous formation in the 
thoracic cavity involving the mediastinum, pericardium, pleura 
and some smaller nodules in the lung. (The lung nodules were, 
no doubt, metastatic formations.) Because of their tendency to 
form metastases and the rapid peripheral infiltration these tu- 
mors usually cause a fatal termination. 

Lympho-sarcomata are a variety of round-celled sarcoma, and 
are called lymphomata by some authors. They are quite com- 
» mon in all domestic animals. These tumors have their origin 
in lymphoid tissue and are extended by the lymph. Two cases 
have been studied in the ox in which the primary lesion was in 
the wall of the abomasum. One case of generalized lymphosar- 
comatosis has been observed in a chicken. A pericardial lym- 



304 



VETERINARY PATHOLOGY. 



phosarcoma was found in a post-mortem examination of a sheep. 
An omental lymphosarcoma in a dog was reported in the Ameri- 
can Veterinary Review, December, 1905. The color, consistency 
and size of lymphosarcomata is quite variable. 

Microscopically these tumors are found to be composed of 
lymphoid cells, the tumor cells being supported by stellate cells. 
Lymph vessels are usually quite numerous and their structure is 
similar, if not identical, to that of normal lymph vessels. The 
stellate supporting cells and the presence of lymph vessels are 
the distinguishing characteristics of lymphosarcomata. There 
is no leucocytosis in animals affected with lymphosarcomata, 
while in those affected with leukemia leucocytosis is well marked. 

These tumors are malignant. They form metastases through 
the lymph and blood channels. They are usually surrounded by 
a very thin capsule. 





Fig. 159. — Photograph of a mule affected with a spindle cell Sarcoma of tlie eyelids. 
1. Granular denuded tumorous surface. 2. Granular funproid tumorous mass. 



TUMORS. 



305 



Spindle-Cell Sarcoma. — Tumors of this variety are composed 
of spindle-shaped cells. They are more firm and dense than the 
round-cell sarcomata. These tumors are not rare, occurring 
most frequently in connection with the skin or subcutaneous 
tissue. Some of the resistant and incurable cases of fistulous 
withers are spindle-celled sarcomata. A collar boil that did not 
respond to treatment was found to be a spindle-cell sarcoma. 
These tumors are common in the eyelids of horses and mules 
and are sometimes quite resistant to surgical interference. The 






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Fig. 160. — Section from spindle cell Sarcoma of a mule's eyelid. 



cells vary from short, thick fusiform cells to elongated fibre-like 
cells. Spindle cells are more matured than the cells of round- 
cell sarcoma. Round cells have no tendency to become spindle 
cells, neither do spindle cells become either round cells or ma- 
tured connective tissue cells. The cells in spindle-cell sarcomata 
have no definite arrangement but extend in all directions. In 
microscopic section some cells are cut transversely, others ob- 
liquely, and still others longitudinally. Hence we find the 
nucleus is centrally located, is usually spherical or oval in shape, 
and is not as large in proportion to the size of the cell as that 
of the round cells. Some have suggested a classification of this 



306 



VETERINARY PATHOLOGY. 



group into large and small-celled varieties. The cells are usu- 
ally held together by reticular connective tissue. This may be 
demonstrated in sections in which the sarcoma cells have been 
dissolved out by acetic acid. The density of the tumor depends 
upon the relative quantity of protoplasm the cells contain and 
the amount of intercellular material. A tumor composed of 
short, thick spindles is less dense than one composed of fibre- 
like cells. Blood vessels usually have normal vessel w^alls and 
are not as numerous as they are in round-cell sarcomata. 







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Fig. 161. — Myeh.id or Giant cell Sarcoma of the Humerus. 

a. Giant cells. b. Sarcoma cells. 



These tumors are usually encapsulated, rarely form metas- 
tases and are, in general, not as malignant as the round-cell 
variety. They may be mistaken for fibromata, but a careful 
study of a microscopic section is usually sufficient for differen- 
tiation. Fibromata contain no elements that appear like trans- 
verse sections of spindle cells. Leiomyooia may be dift'eren- 
tiated by the shape of the nucleus and the selective action of 
stain as picrofuchsin. 

Myeloid-Cell Sarcoma (Giant-Cell Sarcoma). — This is a 
variety of sarcoma characterized by the presence of myeloid or 
large multinucleated giant cells (myeloplaxes). Surgeons and 
pathologists frequently find myeloid sarcomata in man, but they 
are rare in domestic animals. Thc}^ are invariablv found in 
relation to, or in connection with, bone-marrow, or more rarely 



TUMORS. 



307 



in relation with periosteum. They frequently contain cartilag- 
inous, osseous or calcareous centres. 

Microscopically, they are composed of myeloid cells and 
round or spindle cells. The myeloid cells are the distinguishing 
elements of this variety o.f sarcoma. The size of the myeloid 
cells is variable, frequently being 80 to 100 microns in diameter 
and with an irregular outline, varying in shape from a sphere to 
an elongated mass. Their protoplasm may be quite granular or 
almost clear. They have many nuclei — 150 being observed in 
one cell. These nuclei have no definite arrangement but occur 
miscellaneously throughout the entire cell body. The round and 
spindle cells are like those occurring in round and spindle-cell 




Fig. 162. — Photograph of horse's head affected with mixed cell Sarcoma. 



sarcoma. There may be an excess of one or the other or they 
may be equal in number. The intercellular substance varies 
from mucoid to calcareous in nature. There is usually an exces- 
sive blood supply, the blood vessel walls being usually normal 



VETERINARY PATHOLOGY. 

in structure. Degeneration as well as necrosis and calcification 
are of frequent occurrence in myeloid sarcomata. 

These tumors may not be completely encapsulated, though 
there is always a tendency for them to be circumscribed. They 
are the least malignant of all sarcomata. They rarely form me- 
tastases. 

Mixed-Cell Sarcoma. — This is a variety of sarcoma charac- 
terized by the presence of variously shaped cells, as round, spin- 
dle and even stellate cells. This variety is not as common as 
either the round-cell or spindle-cell varieties. They have been 
observed in the horse, hog and ox, but they doubtless occur in 
all domestic animals. They affect bone, glandular tissue, and 
meninges of the brain, in fact, no tissue is exempt. An inter- 
esting case of mixed-cell sarcoma of the inferior maxilla of a 
horse was described in the December Veterinary Review, 1905. 
The tumors frequently degenerate and become necrotic. Mi- 
croscopically they are composed of round cells and spindle 
cells that are identical in structure with those described in the 
discussion of round-cell and spindle-cell sarcomata. Stellate 
cells may be present, and are very similar in structure to mucoid 
connective tissue cells. The cellular elements are supported by 
reticular tissue or by fibrous connective tissue. The number of 
blood vessels is variable. There is an excess of vessels in those 




Fig. 16'3. — Photograph of Maxilla of horse shown in Fig. 162. showing 3 bony points; 
the remainder of the maxilla being completely destroyed by the sarcomatous tissue. 



TUMORS. 



309 



made up principally of round cells and in those that have a lim- 
ited amount of intercellular substance. The vessel walls may 
be normal or they may be composed of sarcomatous tissue. De- 
generate or necrotic changes in the tissue necessarily alter the 
microscopic appearance. 








Fig. 164. — Section of a mixed cell Sarcoma of the inferior maxilla of a horse. 



These tumors are usually diffuse ; that is, they are not encap- 
sulated. They form metastases, and hence are malignant. 

Alveolar Sarcoma. — This is a sarcoma characterized by the 
arrangement of the sarcoma cells into groups or nests, and is 
occasionally found on domestic animals, especially in the ox and 
hog. The reproductive glands, ovary and testicle, are the struc- 
tures most frequently invaded by them. They may become 
quite large. An alveolar sarcoma obtained from the ovary of a 
heifer weighed 15 kilograms (33 lbs.) and was about 20 cm. (8 
in.) in diameter. 

Microscopically the cells are usually round, although they 
xnay be spindle-shaped. The stroma of the tumor is made up oi 



310 



VETERINARY PATHOLOGY. 



two portions. One portion is usually composed of spindle cells 
which are connected into dense bands extending in various direc- 
tions and forming alveoli ; hence the name alveolar. The other 
portion of the stroma is intercellular and corresponds to that of 
the round-cell sarcoma. The arrangement of the cells into nests 
is suggestive of a carcinoma, but the differentiation is not diffi- 
cult and depends upon; first, the presence of intercellular sub- 
stance between the cells which is present in sarcomata but is 
absent in carcinomata ; second, sarcomatous cells are embryonic 
connective tissue cells and hence contain nuclei relatively large 
in proportion to the size of the cell, while carcinomatous cells are 
embryonic epithelial cells and contain nuclei relatively small in 
proportion to the size of the cell. 




Fig. 165. — Section of Alveolar Sarcoma from u\aiy of heifer showing alveoli filled 

with sarcomatous cells. 



These tumors grow slowly. They are usuallv encapsulated 
and have no tendency to form metastases. Thc}^ are very mildly 
malignant. 

Enthothelioma is a tumor composed of endothelium. This is 
a tumor that is not specifically a sarcoma, but may be so classed. 
Endothelium has the same ori2;in as connective tissue, i. e.. the 



TUMORS. 



311 



mesoderm. Embryonic endothelial cells are structurally iden- 
tical with embryonic connective tissue cells. These tumors are 
not very common in domestic animals. An endothelioma was 
observed in the lung of a dog, another in the testicle of a bull. 
These tumors may have their origin from the endothelium lining 
blood or lymph channels, peritoneum, pleura, pericardium, arach- 
noid membrane, any organs developed from mesothelium, or 
deflections from any of them. They are variable in shape, size, 
color and consistency. 

Microscopically they are composed of cells that most fre- 







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Fig. 166. — Section of Endothelioma from a bull's testicle. Note the bands of 
connective tissue and arrangement of cells. 



quently resemble sarcoma cells, although they may approximate 
the structure of carcinoma cells. The cells may be arranged 
in tubules, transverse or oblique sections appearing as sections 
of gland tubules or acini. If arranged in columns transverse or 
oblique sections appear as cell nests. The cells are usually 
cubical or spherical in shape, although they may be spindle or 
even squamous. The stroma varies according to the tissue in- 
vaded and may be dense fibrous or mucoid. Blood vessels are 
usually quite numerous, and if the endothelium is derived from 



312 



VETERINARY PATHOLOGY. 



the endothelium of a vessel, the vessel may be very irregular i 
calibre and structure. If the cells occur in columns or nests i 
will be necessary to differentiate them from carcinomata. Thi 
differentiation involves the comparison of cells derived fror 
mesoderm and those derived from entoderm or ectoderm. Th 
only essential difference, and that is not constant, is the size c 
the nucleus. The differentiation may also be governed to som 
extent by the distribution of the blood vessels. If the cells occu 
in tubules, their differentiation from the adenoma will be neces 
sary. Adenomata may be differentiated by observing the same 




Fig. 167. — From drawing of a Nodule of a Mediastinal endothelioma. 
Column of endothelial cells. 2. Diffuse mass of endothelial cells. 



factors that are used in differentiating endotheliomata from car- 
cinomata. Alveolar sarcomata are very difficult to differentiate 
from endotheliomata, in fact it is sometimes impossible. 

These tumors are not encapsulated and usually form meta- 
stases. They usually occur in internal organs and hence surgical 
relief is impossible. Fatal termination is the usual outcome. 

Fibrosarcoma. — This is a tumor composed of both adult and 
embryonic connective tissue. They are quite common, espe- 
cially in the eyelids and in labial commissures of horses and 



TUMORS. 



313 



mules. Several cases of dense tissue growths in the withers 
of horses have been observed. These animals when presented ap- 
peared to be affected with chronic inflammation of the subcutan- 
eous tissue or deeper structures. Most of the above cases were 
clinicallv diagnosed as fistulous withers and an operation recom- 
mended. The operation usually consisted of dissecting away 
the dense masses of tissue. The ca^es were usually returned in 




Fig. 168. — A so called grape sarcoma from uterus of a cow. 



314 



VETERINARY PATHOLOGY. 



from four to six weeks after the operation with growths larger 
than those present before the operation. The operation was 
usually repeated two or three times with the same results. 

On microscopic examination these growths were found to be 
fibrosarcomata, being composed principally of fibrous connective 






Fit 



169. 



-Photograph showing 31elanotic tumor superior to anus. 



tissue in which there were some spindle cells and occasionally a 
few round cells. The presence of both fibrous and sarcomatous 
tissue is the principal characteristic of these tumors. The num- 
ber, size and distribution of blood vessels are very irregular. 

These tumors are not distinctly encapsulated, but they do not 
form metastases. They are prone to recur after ablation. They 
may destroy life after a considerable time, as their growth is 



TUMORS. 



315 



relatively slow. Operation usually stimulates them to grow 
more rapidly. 

Melanosarcoma. — A melanosarcoma is any variety of sarcoma 
in which melanin is deposited in the tumor cells. These tumors 
are quite prevalent. Gray horses seem to have a special predis- 
position to them, but thev are also found in bay and black horses, 
black or red cattle, black hogs, and, in fact, all varieties of do- 




Fig. 170. — Melano Sarcoma of hog skin. 



mestic animals regardless of color. On microscopic examination, 
melanin is found deposited in the tumor cells. The melanin may 
be in masses or granular and occasionally it mav be found out- 
side of the cells. Excepting the deposit of melanin, these tumors 
have the same microscopical appearance as the round or spindle- 
cell sarcomata described before. 



316 



VETERINARY PATHOLOGY. 



Melanotic sarcomata are frequently malignant. In an autopsy 
of a gray mare metastases of melanosarcomata were found in the 
liver, lung, spleen and kidney, the primary growth being located 
in the subcutaneous tissue on the right superior portion of the 
anus. Another case was observed in which there was general- 
ized melanosarcomatosis in a short-horn cow. 

Myxosarcoma. — This is a tumor composed of myxomatous 
and sarcomatous tissue. The existence of this group of tumors 






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Fig-. 171. — Section of Melano Sarcoma of a horse's liver, showing- the 
deposit of melanin in the tumor cells. 



is doubted by some pathologists because sarcomata are prone to 
undergo mucoid degeneration, and, because if the mucoid degen- 
eration is of limited extent and generalized throughout the en- 
tire tumor, differentiation would be practically impossible. If 
the mucoid degeneration afifects localized areas the differentia- 
tion is not difficult. One myxosarcoma has been studied. It in- 
volved the right lobe of the liver of a cow but was not the cause 
of death. The tumor, about the size of a goose egg, was encap- 
sulated, soft and pale pink in color. 

Microscopically it was composed of stellate cells, the pro- 
cesses of which were apparently united, thus forming alveoli. 



TUAiORS. 



317 



There were also round cells, some areas being composed almost 
entirely of round cells and others of stellate cells. The round 
cells were like the round cells found in sarcomata. The alveoli 
formed by the stellate cells were filled with a stringy mucus ma- 
terial. A few blood vessels were observed but they were not as 
numerous as in pure sarcomata. 

These tumors may be malignant. When they occur upon or 
near available surfaces they usually become necrotic, slough and 
produce no further trouble. 




Fig. 172. — Section of a Myxo-Sarcoma, from a cow's liver, showins 

1. Spaces formed by the union of the processes of the stellate cells. 

2. Sarcoma cells. 



Chondrosarcoma and tumors composed of chondromatous and 
sarcomatous tissues are not common. They usually occur in 
the location most favorable for chondromata. A chicken affected 
with a chorulrosarcoma of the sternum was obtained at a butch- 
er's stall at the city market in Kansas City recently. 

Microscopically, these tumors are found to be composed of a 
mixture of chondromatous and sarcomatous tissues in varying 
proportions. Sometimes the chondromatous tissue is apparently 
stroma for the sarcoma tissue proper. In other cases the stroma 
is apparently formed of sarcomatous tissue and the chondro- 
matous tissue is the essential portion of the tumor. 



318 VETERINARY PATHOLOGY. 

These tumors may grow to an enormous size. They are not 
as malignant as pure sarcomata and metastatic tumors are rare. 
They should be differentiated from chondrofying sarcomata and 
from sarcomata involving cartilage. 

Osteosarcoma. — This variety of tumors is composed of 
osseous and sarcomatous tissues. They are rather common, 
occurring in the horse, dog and ox. 

Microscopically, osteomatous and sarcomatous tissues are 
arranged in various proportions and in various relations, but 
the combining tissue in any case must be new growth tissue. 
Ossifying sarcomata are not osteosarcomata, neither are sarco- 
mata of osseous tissue osteosarcomata. 

These tumors are. usually malignant, but they do not form 
metastases. 

Hemangiosarcoma. — These tumors are composed of heman- 
giomatous and sarcomatous tissues. They are relatively com- 
mon, occurring in the location common for haemangiomata and 
may affect any of the domestic animals. These tumors are essen- 
tially very vascular and are highly colored. 

In microscopic examination variations are observed in differ- 
ent hemangiosarcomata. The sarcomatous tissue in some cases 
appear to have had its origin from the tunica adventitia of the 
vessel wall ; in other cases the sarcomatous tissue appears to 
have had its origin independent of the vessels. Again, the ves- 
sels may act as the supporting stroma for the sarcomatous tissue. 
The vessels may be capillary or cavernous, sinusoid or plexiform. 
The vessel wall may be practically normal, but more frequently 
it is either hypertrophied, as a result of increased number ot 
the cellular elements or increase in the size of the cells, or it 
may be thin, scale-like and atrophied. Sometimes the endothe- 
lial cells lining the vessels are cubic or columnar in shape, thus 
diminishing the lumen of the vessel. The sarcomatous cells may 
be either spindle-shaped or round. 

These tumors are quite malignant, and they usuallv groAV 
rapidly. The metastatic tumors are most frequently pure sarco- 
mata. 

PAPILLOMA. 
(Warts.) 

Papillomata are fibro-epithelial tumors. These are perhaps 
the most common of all tumors. They occur upon the surface of 
the skin, and upon mucous, serous, and synovial membranes. 
They are very common upon the skin of calves, especially around 
the eyes, ears and poll. They occur most frequentlv on the lips, 



TUMORS. 



319 



buccal mucous membrane, and arms of dogs. The skin of the 
legs and lips are the common locations in the horse. The lumen 
of the oesophagus of the ox may be almost occluded by the pres- 
sence of masses of papillomata. In a horse used for dissecting 
the cardio-pyloric junction was found to be a mass of these 
tumors. The mucous membrane of the bladder of the ox, sheep 




Fig. 173. 



-From photograph showing- Papillomatosis of mucous membrane 
of lips of a horse. 



and hog is sometimes studded with papillomata. These tumors 
have also been observed upon the combs and wattles of fowls. 
They sometimes occur in horses' feet but are usually necrotic 
and do not have the appearance of papillomata. 

These tumors may be hard, i. e., covered over by stratified 
squamous epithelium that has become cornified. This variety is 



320 



VETERINARY PATHOLOGY 



invariably found upon the skin and constitutes the grow^ths ordi- 
narily known as warts. They may also be soft, and are then 
found upon mucous, serous or synovial membranes, in which 
case the covering epithelium is not cornified. Hard papillomata 
or warts may appear as tabulated masses, as fungoid growths or 
as a mass of villi. Any of the above forms may have a smooth 
surface or be fissured with a very irregular surface. They vary 
in size from a millet seed to an apple. They may be single but 
are more frequentl}^ multiple. 

Microscopically, they are composed of adult epithelium and 
of fibrous connective tissue in varying proportions. They sug- 
gest the structure of cutaneous papillae. In fact, they have been 



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ouffse 



Fig. 174. — Section of Papilloma from Oesophag:us of cow, showing 
bands of stroma covered by epithelium. 



described as hypertrophied papillae. The fibrous tissue is the 
supporting structure or framework of the tumor and contains 
the blood vessels and nerves when they are present. The epi- 
thelium is the covering mantle of the fibrous tissue. In the hard 
papillomata the epithelium is stratified and the surface cells are 
cornified. In soft papillomata the epithelium may be single or 
stratified but the surface cells are not cornified. The proportion 
of fibrous tissue and epithelium in papillomata may be the same 



TUMORS. 321 

as in normal papillae or the fibrous tissue or the epithelial tissue 
may be in excess. Hence some papillomata are apparently sub- 
epithelial fibromata and others are masses of epithelial cells 
upon a very limited fibrous matrix. Papillomata have the 
same relation to underlying structures that normal papillae 
have. The stroma of the papillomata has a definite connection 
with the dermis in cutaneous papillomata and the epithelium 
apparently originates from the lower layers of the epidermis. 
Transverse sections appear as areas of stroma surrounded by 
epithelial cells, while epitheliomata are composed of columns of 
cells surrounded by a stroma. 

These tumors are essentially benign. They mav result fatally 
because of mechanical interference, as in the occlusion of the 
oesophagus or the urethra. They may undergo necrosis, thus 
providing an entrance for infection and result in fatal septicemia. 
Papillomata do not form metastases, but they are frequently 
multiple. Cases have been recorded where the condition papil- 
lomatosis has been transmitted from one animal to another. By 
constant irritation some epithelial cells may become enlarged in 
the subsurface, thus providing a centre from which an epithe- 
lioma may develop. They respond to medicinal treatment and 
surgical interference. 



EMBRYONIC EPITHELIAL TUMORS. 

This is a group of tumors composed of embryonic epithelial 
cells, and for description may be divided into three varieties, — 
(1) carcinoma, (2) epithelioma, and (3) adenoma. 

Carcinoma is an epithelial tumor characterized by the group- 
ing of cells into nests or alveoli. They are of rather common 
occurrence but not as common as sarcomata. Horses and mules, 
cattle, sheep, hogs and dogs have been observed affected with 
carcinomata. These tumors have no selective action for any 
tissue. They have been found aft'ecting mucous membranes, 
glandular structures, invading muscles and even in bone. They 
are usually diffuse, although they may be limited by a membrane 
resulting from reaction of the surrounding tissue. They are 
usually soft (encephaloid), but they may be quite hard (scir- 
rhous), depending upon the amount of stroma or fibrous tissue 
contained. The color of a cut section of a carcinoma is usually 
gray, dirty-white or pale pink. They may be mottled because of 
degenerating or necrotic centers or hemorrhage. Lobules may 
be observed, especially in those carcinomata formed by the eel- 



2>22 



VETERINARY PATHOLOGY. 



hilar infiltration into dense areolar tissue. Small blood vessels 
may be present, but the blood supply is usually very limited and 
the vessels occur only in the stroma. 

Microscopically, these tumors are found to consist of embry- 
onic epithelial cells arranged in nests, the cells having no inter- 
cellular substance betv^^een them. The cells are variable in size 
and in shape, they may be squamous, spherical or columnar. The 
nucleus is usually much smaller in proportion to the size of the 
cell than the nucleus of sarcoma cells. The stroma is usually 




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s "ft? 



Fig. 175. — Section of Maxillary Carcinoma of a *iorse, showing the nest 
of epithelial cells surrounded by a stroma. 



appropriated from the pre-existing tissue and therefore is vari- 
able in quantity and structure. In some cases sarcomatous tissue 
constitutes the stroma. The stroma forms alveoli in which the 
carcinoma cells occur. In fact, the alveoli are, in many instances, 
simply dilated lymphatic spaces v^hich have been invaded by 
carcinoma cells. Lymph is usually quite abundant and bathes 
the nests of the carcinoma cells in the alveoli. Because of the 
freedom of anastomosis of lymph spaces and the constant flow of 
lymph, carcinoma cells are easily and rapidly diffused. Karyo- 
kinetic figures are of common occurrence in rapidly growing 
carcinomata. There is usually an inflammatory reaction accom- 



TUMORS. 



v> . v) 



panied by a leucocytic infiltration in the adjacent tissue. In rap- 
idly growing carcinomata the cells frequently completely ob- 
struct the flow of lymph through the alveoli, resulting in degen- 
eration or necrosis. Mucoid degeneration is perhaps the most 
frequent variety, thus producing a mucous mass. 

Clinically, these tumors are malign. They are not circum- 
scribed, hence their extirpation is practically impossible. In fact, 
surgical interference usuall)^ stimulates them to more rapid de- 
velopment, and, in addition, opens an avenue for infection. They 




Fib. 176. — Section of an Enitlielioma of the hock of a hois.: n'-as th>' sequel 
of an injury. Note the ingrowth of the columns of epithelial cells. 



form metastases. The metastatic tumors usually occur in the 
first lymphatic gland that the lymph passes through from the 
area affected with the carcinoma. Then by metastasis they will 
be extended on to the next group of glands and finally reach the 
blood stream and form carcinomatous emboli in the lungs, 
liver, etc. 

These tumors should be differentiated from alveolar sarco- 
mata, endbtheliomata and papillomata. The sarcoma has a much 
larger nucleus in proportion to the size of the cell and the cells 
are usually smaller than carcinoma cells. In a cross-section of a 



324 



VETERINx\RY PATHOLOGY. 



papilla from a papilloma the cells will be found arranged around 
the stroma instead of in nests as in carcinoma. 

Carcinomata are sometimes associated with other tumors as 
fibromata and chondromata, but they are more frequently in 
combination with sarcomata, in which the sarcomatous tissue 
forms the stroma of the carcinoma. The sarcoma cells are usually 
of the spindle-celled variety. 

Epithelioma. — This type is the result of an ingrowth of epi- 
thelium into the underlying structures and has been classed by 
some as a sub-variety of carcinomata. In this variety of tumors 




there is considerable evidence that they are secondary to 
surface injuries. A horse with a large fungoid growth beneath 
the left eye was sent to a Kansas City veterinarian for treatment. 
The history of the case brought out the fact that the tumor was 
the sequel of a wire cut. Two similar cases of epitheliomata oc- 
curred in the eye of two cows after severe attacks of keratitis. 
Epitheliomata are not rare and may affect any of the domestic 
animals. They always occur primarily in relation to epithelial 
surfaces. The surface is usually denuded and there is usually 
an acrid, fetid discharge. They may appear as elevated nodular 



TUMORS. 



325 



masses or as ulcerated surfaces and are rarely encapsulated. 
Their consistency varies with the amount of connective tissue 
stroma present. Their color is usually white or gray, although it 
may be quite variable as a result of degeneration or necrosis. 
The quantity of blood depends upon the vascularity of the tissue 
invaded. 

Microscopic sections of epitheliomata are usually very similar 
to carcinomatous sections, indeed, it is sometimes impossible to 
differentiate them from carcinomata. In the beginning of the 
tumor formation, if sections are made perpendicular to the sur- 









^^ ,__jj; -/^•■, -^ --^ v.\^-;v ,j 







mm 



I'ig. 178. — Section of a pearl cell Epitholionia of the Subcutuni of a 14-year-old 
dog, showing pearl cells and columns of epithelial cells. 

face, the ingrowing epithelium will be observed as columns of 
cells. These cell columns extend into the areolar lymph spaces 
and are then distributed the same as in carcinomata, the pre- 
existing tissue stroma becoming the stroma of the tumor. The 
presence of the epithelial cells or their katabolic products some- 
times produces a chronic inflammation of the stroma. The pres- 
sure produced from the thickened stroma upon the columns of 
epithelial cells may result in the formation of '"pearls." Epithe- 
liomata containing the ''pearls" are designated pearl-cell epithe- 
liomata. 



326 



VETERINARY PATHOLOGY. 



Clinically these tumors are not as malignant as carcinomata 
proper, and they have less tendency to form metastases. They 
are frequently completely destroyed by surgical interference. 

Adenoma. — This is a glandular tumor. While it is similar 
to a gland it is functionless or has a perverted function. Though 
occurring more frequently in glands, as the kidney, mammae, mu- 
cous or sebaceous glands, testicle, liver, etc., they may occur in 
any tissue. Swine and dogs are most frequently affected with 
them. They are usually circumscribed, rather firm, nodular, 
white or grayish-white masses, varying in size from a pea to a 






Fig. 179. — Photograph showing Mammary Adenoma of a bitch. 

man's head. In section the gross specimen usually appears lobu- 
lated, and, if the tumor is large, there are usually necrotic centres 
here and there through it. The blood supply is limited, the ves- 
sels usually being obstructed by the pressure of the new-formed 
adenomatous tissue. 

In microscopic sections glandular cells are found in various 
arrangements as tubules, acini, etc. The mimicry, however, is 
not complete, and there is usually little difficulty in differentiat- 
ine adenomata from normal gland tissue. The cells varv in 
shape from short cubical to tall columnar. They are usually 



TUMORS. 



Z27 



arranged in a single layer, although the tubules or acini may be 
entirely filled with cells arranged layer upon layer. The type 
of cells adheres to the description given in discussing carcinoma. 
The stroma is usually composed of fibrous connective tissue 
and is variable in amount. Blood vessels are found within the 
stroma. The cells lining the acini may be active and the secre- 
tion is frequently retained, thus resulting in a cyst-adenoma. 
The accumulated secretion may cause degeneration of the stroma, 
and the acini rupturing one into another produce a large cyst. 




Fig. ISO. — Section of an Adenoma from the frontal sinus of a mule, showing 
the arrangement of tumor tissue into acini and tubules. 



Clinically these tumors, as a class, are malignant, but do not 
produce fatal results as rapidly as carcinomata. Many individ- 
ual adenomata are benign. A horse's tail was recently ampu- 
tated that for three years had been affected with an adenoma of 
the sebaceous glands. A bitch affected with an adenoma of the 
mammary gland has been under observation for two years and 
is normal except for the presence of the tumor. These tumors 
rarelv recur when removed. From experience it has been found 
that mammary adenomata of the bitch usually result fatally im- 
p-'^diatelv after operation. (The operation appears to produce 



32S 



VETERINARY PATHOLOGY. 



sufficient shock to destroy life.) Adenomata are extended by 
means of the lymph. Various combinations of adenomata are 
common. 

Adeno-Sarcoma. — This is a tumor composed of adenomatous 
and sarcomatous tissue. These tumors are seldom observed dur- 
ing life because they occur in the kidney, and it is not an easy 
matter to palpate the kidney in the domestic animal unless there 
is extreme emaciation. They usually affect only one kidney. 
They occur in young animals and are most common in the hog 
although one has been observed in a horse. These tumors grow 
ra])idly and may become very large. Day reported one that 
weighed 27.2 kilograms (60 lbs.) found in the kidney of a hog. 

Renal adenosarcomata usually have their origin near the kid- 
ney pelvis. The renal tissue is gradually displaced by the tumor, 
and in some instances the kidney tissue is entirely destroyed as 
a result of pressure atrophy. The tumors are usually confined to 
the kidney, but they form metastases, in the lung (through the 
blood, or in the sublumbar lymph nodes (through the lymph.) 

In gross appearance, these tumors are irregular in outline. 
They are usually surrounded by a thin fibrous capsule from 
which fibrous bands project into the tumor dividing it into 







2. .es o* '><» ^^-N 



K'^llfj^n^^f^ 



Fig ]8]. 



-Section of an Adeno-Sarooma of the kidney of a hog, showing the 
sarcomatous tissue between the acini and tubules. 



TUMORS. 



329 



irregular lobes. These tumors are usually mottled, though they 
may be uniform and of a white or light gray color. 

Microscopically, adenosarcomata are composed of epithelium 
and connective tissue. The amount and arrangement of the two 
types of tissue are variable. Some areas may be entirely epi- 
thelium (adenomatous) and other areas connective tissue (sarca- 
matous). The epithelium is arranged as grandular tissue, 
the tubes and acini of which are irregular in shape and size 
and may contain disintegrating, epithelial cells or their products. 
The epithelium is usually arranged in a single layer in the tubes 
and acini though they may be grouped in some instances and 



















Uj'/i. 



.-»■/ 



Fig. 1S2 — Section of a Cystadenoma of the mammary gland of a sheep, showing: 
1. Coagulated cystic contents surrounded by an atrophied acinous wall. 



thus appear similar to carcinomatous nests of cells. The epithe- 
lial cells are small and usually contain finely granular chromatin. 
The connective tissue cells are usually fusiform although they 
may be nearly spherical in shape. They contain relatively large 
nuclei in which granules may be observed. 

Cystadenoma is also common, especially in those adenomata 
that produce secretion. They are found in the adenomata of the 
mammary and sebaceous glands. 

Hypernephroma are tumors which may be classed either with 



320 



VETERINARY PATHOLOGY. 



sarcomata or carcinomata and is composed of tissue similar to ad- 
renal tissue. They occur most frequently in the kidney, ovary, 
or adrenal body itself. Hypernephromata are rarely diagnosed 
as such in living domestic animals. They are variable in size, fre- 
quently weighing as much as five kilograms (11 lbs.) Usually 
gray in color and invariably containing hemorrhagic areas they 
thus appear mottled. There is usually an encapsulating mem- 
brane present. Blood-vessels are numerous, especially in the 
stroma. Degeneration and necrosis is of common occurrence. 







" ja' 'tL\ -.<. '■-to'^ii^' -c^^^^T*^ j;^^?^^-" ) -"^^ 



Fig. 183. — Hypernephroma of the kidney of an ox, showing large> typical hyperne- 
phromatous cells containing fat droplets. 



Microscopically, these tumors are found to be made up of 
large cells similar to epithelial cells and usually containing fat 
droplets. These cells are arranged in rows or columns, the 
columns being separated from each other by a small amount of 
stroma. The columns of cells may be quite variable in their 
diameter, appearing at times as long, slender columns and again 
as rather long nests of cells. The stroma is composed of fibrous 
connective tissue and contains many blood-vessels. 

Clinically, these tumors are very malignant, and, although 



TUMORS. 331 

they are encapsulated, they form metastases through the blood. 
They usually result fatally in the human, even after operation, 
probably because of the liberation of considerable of the adrena- 
lin substance which increases blood pressure to such an extent 
that heart failure supervenes. 

PLACENTOMA. 
(Syncytioma.) 

A placentoma is a tumor composed of tissue similar to the 
chorionic villi. 

These tumors have been described under a variety of names 
as syncytioma malignum, deciduoma malignum, chorio-epithei- 
ioma, epithelioma seritonale, chorio-carcinoma. Only recently 
have placentomata been recognized as distinct tumors. 

A placentoma is essentially a tumor of the uterus. They are 
not common in domestic animals but this may be because of fail- 
ure to recognize them. The uterus or fallopian tube is their 
most frequent location. They occur more frequently after spur- 
ious or mole-pregnancy and usually appear a short time after 
parturition. Abortion is a predisposing cause. The primary 
tumor almost invariably occurs in the uterus though a few cases 
have been reported in women in which the primary tumor was 
in the kidney. They are very malignant. 

These tumors appear as soft, spongy, villous, bleeding masses 
and are variable in size. They have the general appearance of 
placenta or foetal membranes in both the primary and the metas- 
tatic tumors. They begin to develop at the cotyledons or zone 
of placental attachment and rapidly extend into the uterine mus- 
cular tissue and invade blood vessels, thus metastases occur 
in a short time after the tumor appears. Because of their struct- 
ure (embryonic cells and rich vascular supplv) thev grow rap- 
idly. 

The presence of a placentoma is indicated by uterine hem- 
orrhage occurring a few days after normal parturition or abor- 
tion. The uterus is enlarged and the affected individual rapidly 
becomes anemic and emaciated. The uterine discharge usually 
contains shreds of the tumor and the cavity of the uterus is 
occupied with a soft bleeding mass. 

Microscopically, these tumors are composed of a protoplasmic 
ground-substance, which is arranged in an irregular network 
forming alveoli. The protoplasmic mass is usually continuous, 
there being no evidence of cell partitions, and it contains many 
nuclei thus forming a syncytium. Within the alveoli of the pro- 



2>2>2 



VETERINARY PATHOLOGY. 



toplasmic mass occur many small variously shaped cells. Blood 
cavities and canals are abundant and hemorrhagic areas are not 
uncommon. 

TERATOMA. 

These tumors are composed of the different kinds of tissues that 
approximate the structure and arrangement of normal tissue so 
closely that it is difficult to differentiate them macrosopically or 
microscopically from normal tissues and organs. Teratomata 
are so closely related pathologically to malformation, that in 
some cases it is impossible to determine which condition exists. 
Structurally they are found to be composed of either embryonic 
or adult tissues. Cutaneous structures are the most frequent tis- 
sues observed in this class of tumors, although tissues of bone, 
muscle, intestine, rudimentary eyes, brain, etc., have been found 
in them as well as sarcomatous and carcinomatous tissue. 




Fig. 184. — Dermoid Cyst from the withers of a horse. 



These tumors are quite variable in size, shape and color. In 
consistency, they vary from a viscid mass to dentine and enamel. 
They are usually single, grow slowly and rarely form metasta- 
ses, although a few have been observed that grew rapidly, metas- 
tasized and recurred when removed. They frequently undergo 
degeneration tending to cystic formation. Clinically, teratomata 
are benign, only rarely terminating fatal-v. 

Etiologically, they are as mysterious as the other types of 
tumors. They may have their origin from tissue inclusions. 
Some teratomata mav succeed imperfect tissue union. The the- 



TABLE I. 



Myxoma, chondro 



Connective. < 



Osteoma, odontoma. 
Lipoma, glioma. 



L Fibroma- 1 



' ^^w^^ tissue. ^ Epithelium 



y Papilloma. 



J 



Muscular — Myoma J Leiomyoma. 

I Rhabdomyoma. 

Vascular — angioma J ^^^(^ngioma. 

] Lymphangioma. 

I Nervous — neuroma. 



Connective — Sarcoma 



f Round cell. ^ 



Spindle cell. 



Myeloid cell. 



r s^ 



L Embryonic tissue. 



Endothelioma. Hypernephroma. 



I 



Carcinoma. 



I F.I itht,hum. •] Adenoma. 



Epithelioma. 



Placentoma. 



TUMORS. 



orv of parthenogenesis may be applicable in the explanation of 
some of them, but the specific cause or causes of teratomata has 
not yet been determined. 

Teratomata are of frequent occurrence in all domestic ani- 
mals but are more prevalent in equines. They are found in any 
tissue and in all parts of the body although they are more fre- 
quent in the skin, ovaries, testicles, kidneys and parotid glands. 




Fig. 185. — Dermoid Cyst from eye of a steer, showing tuft of hair 

growing- upon cornea. 

Because of the heterogenous structure of teratomata they are 
difficult to classify. 

Dermoid cysts are teratomata composed primarily of skin 
and its appendages (hair, sebaceous glands, horn, teeth, etc.) 
They may be solid, but are more frequently cystic. In size they 
vary from a pea to a basket ball. There is usually surrounding 
them a dense capsule from which a villous mass may be ob- 



334 



VETERINARY PATHOLOGY. 



served projecting into the cyst cavity. Extending from the vill- 
ous projection are tufts of hair or teeth. The villus is, in struct- 
ure, very similar to skin. In some teratomata hair and teeth are 
produced directly from the inner portion of the cyst wall. Cys- 
tic dermoids usually contain hair and a pultaceous material de- 
rived from the sebaceous glands or they contain teeth and a vis- 
cid fluid. Dermoid cysts without any capsule are occasionally 
observed. The accompanying cut illustrates hair extending 
from the anterior surface of the eve. Those found in the ovaries 













Fig. 186. 



-Dentigerous Cyst on left inferior maxillary of 3 years old colt 
containing 431 teeth. Removed Dec. 11. 1905, 
by H. M. Stevenson, Perry, Iowa. 



usually contain elements of all three germ layers. Those of the 
testicles may contain vestiges of all the germ layers, but are 
usually cystadenomatous or cystocarcinomatous in type although 
they may contain cartilage, teeth, osseous tissue, etc. Solid der- 
moid cysts are a heterologous mass, of embryonic or adult tissue. 
Dentigerous cyst is the name applied to those dermoid cysts 
containing teeth. These are the most important to the veterin- 
arian because they are of the most frequent occurrence. They 
are invariably encapsulated and may or may not contain a villus 



TUMORS. 335 

projection. The teeth vary from an irregular conglomerated mass 
of dental tissue to those perfect in form and structure. The con- 
stant production and accumulation of the containing viscid fluid 
results in enlargement of the cyst and frequently rupture of the 
capsule and the production of a fistula. The most frequent lo- 
cation of dentigerous cysts is near the base of the ear in the 
region of the parotid gland although they may occur in any 
other place especially in the ovary and testicle. They are most 
common in horses. 

Cholesteatoma is a teratoma composed of pearl like masses 
of epithelium in which there is more or less cholesterin. They 
are not common but have been observed in the brain, (choroid 
plexus and tuber cinereum) and urinary organs. There 
was recently obtained from near the kidney of an ox, a mass of 
substance of a waxy consistency, that gave the typical reaction of 
cholesterin and was probably a cholesteatoma. 



CYSTS. 

DEFINITION. 
ETIOLOGY. 

Retained secretion. 

Obstructed outflow. 

Excessive production in ductless glands. 

Retention of hemorrJiugic extravasate. 

Colliqnation necrosis. 

False bursae. 

Parasites. 
STRUCTURE. 
VARIETIES. 

Retention; Atheroma. 

Exudation; Hygroma, Shoe boil, Capped hock, Meningocele. 

Extravasation; Hematocele, Hematoma. 

Degeneration; Colliqnation necrosis, Hydatiform 

Pa'-asitic; E chinoccosis, Measley pork. 

Dermoid; Cutaneous, Dentigerous 
SECONDARY CHANGES. 
EFFECTS. 

A cyst is a bladder like growth surrounded by a capsule 
and containing a liquid, semiliquid or gelatinous material. Cysts 
are not true tumors. However, a tumor may become cystic, 
(Cystoma,) and the capsule surrounding a cyst may proliferate 
and become a true tumor. Collections of inflammatory and oede- 
matous fluids, are not usually considered as cysts. Cysts may 
be single or multiple. The latter are designated multilocular 
cysts. 

Cause. — Cys's mav be caused by, 1. obstruction of gland ducts, 
thus favo^'n-^ r'^criT.flaticn r^d retention of a normal secretion 



336 



VETERINARY PATHOLOGY. 



or excretion, e. g., renal cysts; 2. By excessive secretion into duct- 
less structures, e. g., distension of bursae ; 3. By extravasation 
into the tunica vaginalis sac, e. g., hematocele ; 4. Liquefying 
necrosis, e. g., formulation of cysts in the cerebrum of horses 
affected with "blind staggers/' 5. Parasites, e. g., Cysticercus 
cellulosae. 

Structure. — The cystic wall varies according to the age of 
the cyst. In the beginning it may represent the original gland 
structure or a condensation of the normal tissue of the part, 
Later the cystic walls may be lined with epithelium or endothel- 
ium, which actively secretes as long as the cyst grows. The cys- 
tic capsule may be composed entirely of fibrous connective tissue. 
In some instances the primary capsule is fibrous and later an 
endothelial lining develops. The cyst Vv^all or capsule may be 




F"".?. 187 — Hctention C^st in crrvical i-ri;i()n of 



TUMORS. 



\Z7 



firmly adherent to the adjacent tissue or it may be loosely at- 
tached. 

The cystic content varies according to the nature of the cyst. 
Urine, milk, saliva, mucus, semen, liquor folliculi and other secre- 
tions and excretions are represented in cystic contents. Blood 
i. e., hemorrhagic extravasates and various tissues that have 
undergone colliquation necrosis may represent the contents of 
cysts. The various secretions, excretions, extravasates, exudates 
and necrotic tissue usually undergo some modification when re- 
tained within a cyst. 

Varieties. — Retention cysts, those resulting from the accumu- 
lation and retention of normal secretions, e. g., ovarian cysts. 
renal cysts, mammary cysts, testicular cysts, ranulae, mucus 
cysts, sebaceous cysts (Atheromata). 




Fig. 188. — Uterine Cyst the capsule of which had become osseous. 



Exudation cysts, those resulting from excessive secretion into 
ductless glands or cavities, e.g., hygroma, capped hock, meningo- 
cele. 

Extravasation cysts, those resulting from hemorrhage into tis- 
sues or closed body cavities, e. g., hematocele, hematoma. 

Degeneration c\sts, those resulting from liquefaction of ne- 
crotic tissue ,e. g. colliquation cerebral cysts. 

Parasitic cysts, those resulting from the development of para- 
sites in the tissue, e. g., cysticercus cellulosae, cysticercus bovis, 
cvsticercus echinococcus, etc. 



338 VETERINARY PATHOLOGY. | 

c 

Dermoid cysts, those resulting from inclusion of cutaneous i 

tissue. These have been discussed under the head of teratomata. i 

Secondary Changes. — The cystic wall may become the seat oi i 
inflammatory disturbances, neoplastic formation or necrosis. In 

some instances cysts are destroyed because of the disintegration j 

of their capsule, by disease. ' \ 

The cystic contents may undergo degeneration, become in- | 

spissated or calcified. | 

Effects. — The effects of cyst formation depend upon the i 

tissue involved and the size and nature of the cyst. The cysts ; 

frequently become so large that the entire organ is destroyed, i 

e. g., ovarian and renal cysts. In some cases the cysts may ] 

destroy life, especially if a vital organ, e. g., the brain is in- j 

volved. Cysts may persist for years and be of no serious con- j 

sequence, on the other hand they may seriously inconvenience ] 

the functional activity of the part involved and impair the health ■' 

of the animal from the beginning. j 



CHAPTER XL 
FEVER 

(Pyrexia). 

DEFINITION. 

ETIOLOGY. — Toxins; ptomains; katabolic tissue products; drugs. 
PERIODS OR STAGES (Course), 
Onset (Stadium Incrementi). 
Acme {Stadium Fastigium). 
Decline (Stadium Decrementi). 
Convalescence. 
VARIETIES, according to 
Course. 

Regular. 
Irregular. 
Duration and temperature variation. 
Ephemeral. 
Continuous. 
Remittent. 
Intermittent. 
Severity. 

Sthenic. ,^ ' 
Asthenic. 
SYMPTOMS. 

Chill, diminished secretious, increased heart action and r^spiraticn, 
nervousness and restlessness. 
LESIONS. 

Parenchymatous degeneration, hemolysis, hyaline degeneration, loss 
of fat. 

Body heat is a product of metabolism. The body heat or 
temperature of warm blooded animals is practically constant, 
although changed environment, diet and use or occupation pro- 
duce some variations. Thus a horse confined in a barn has a 
temperature .5 to 1° F. higher than when not so confined, pro- 
vided the diet is the same in both conditions. A narrow ration 
is conducive to increased oxidation and consequently a higher 
temperature. Animals in action have a higher temperature than 
when at rest. Thus a dog's temperature is from 1 to 1" F. higher 
immediately after than it is before a chase. 

The accurate regulation of body temperature is accomplished 
by the action of the thermo-regulating center or centers. Tissue 
action is always accompanied by increased heat production, and 
frequently difTerent parts of the same animal may vary 1 to 6° F. 
in temperature. The equalization of body heat and the distribu- 
tion of heat to the different parts of the body is accomplished 
by means of the circulating blood. Heat is continually produced 
in the animal body and is constantly eliminated from the bodv 

?30 



340 



VETERINARY PATHOLOGY. 



in the excretions (air, perspiration, urine and feces), as well as 
by direct radiation. The relative amount of heat dissipation by 
the excrements and by radiation varies in different animals. 

Normal temperature is the balance of equilibrium maintained 
betv^een thermogenesis (generation of heat) and thermolysis 
(dissipation of heat). The normal temperature of an animal 
used during the day is about 1° F. higher in the evening than in 
the morning. 

Fever is a condition in v^hich the equilibrium between ther- 
mogenesis and thermolysis has been overthrown, i. e., there is 
a disturbance of metabolism accompanied by increased tempera- 
ture. It is not a disease but a symptom complex, common to 
several different pathologic conditions. Fever should be dif- 
ferentiated from heat stroke and sunstroke. In heat stroke there 
is no disturbance of thermogenesis or thermolysis, but the ther- 
molytic centers are unable to cope with the existing external 
conditions, and there is accumulation of heat in the body, whereas 
fever is a result of disturbed equilibrium between thermogene- 
sis and thermolysis. Sunstroke is a condition produced by the 
action of actinic or chemic rays of the sun upon the nerve cen- 
ters, temperature variations being only a predisposing factor. 

Etiology. — Fever is usually caused by bacterial products 
as toxins, endotoxins and bacterial proteids. Tissue products 
as leucomains, peptones and various albumins are also capable 
of producing fever. Certain therapeutic agents are causative fac- 
tors of fever. 

Course. — The course of a fever may be divided into four per- 
iods or stages, as follows: 

Onset (stadium increment!) is the period of increase between 
the time of normal temperature and the time that the tempera- 





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Fig'. 189. — Charts showing: two fever curves. On the left is given the temperature and 

on the top each number signifies one day or 24 hours. From 1 to 13 is the 

onset; from 13 to 17 and 20 respectively the Acme; from 17 to 32 is 

a gradual decline (lysis); and on 20 is shown a rapid 

declined (crisis). 



FEVER. 341 

ture reaches its average height. The length of the onset and the 

temperature during this period is variable. 

Acme (stadium fastigium) is that period of time that the 
temperature remains high. It is the time from the termination 
of the onset to the beginning of the decline. 

Decline (stadium decrementi) is the time extending from the 
termination of the acme until the temperature reaches the nor- 
mal level. A sudden decline, i. e., when the temperature sud- 
denly changes from acme to normal, is called crisis. In a larg'e 
percentage of the cases of fatal equine pneumonia the tempera- 
ture suddenly drops from the acme to normal, or even subnor- 
mal, the sudden change (crisis) causing death. Excessive varia- 
tions, as a sudden rise of temperature of a sudden fall of tem- 
perature (may be to subnormal) are of rather frequent occur- 
rence a short time before death and is called the moribund or 
premortal stage, A gradual decline from acme to normal is 
called lysis. 

Convalescence is that period extending from the time that the 
temperature becomes normal until the animal has recovered. 
This period varies in length, a long continued fever essentially 
requiring a long period for convalescence. The temperature 
variation during this period is inconstant, but usually there is 
only slight fluctuation from the normal. 

Varieties. — Fevers mav be classified according to course, to 
duration, and to temperature variation as follows : 

According to the course fevers are regular and irregular, typi- 
cal or atypical. A regular fever is characterized by the appear- 
ance of the various stages or periods of fever as described above. 
An irregular fever is one in which the stages are not distinct or 
are not regular in their appearance and duration. 

According to duration and temperature variations, fever may 
be ephemeral, continuous, remittent or intermittent. 

Ephemeral fever is of brief duration, usually lasti^ng not longer 
than 24 hours. It is the type of fever observed in nervous, ex- 
citable animals. This variety of fever may be produced at will 
by some nervous Avomen. 

Continuous fever is that type in which there is a continuous 
high temperature. In continuous fever there are usually morn- 
ing and evening variations the same as in the normal tempera- 
ture. Croupous pneumonia without complications is an example 
of disease in which there is a continuous fever. 

Remittent fever is characteristic of pyemia and is recognized 
by the irregularly periodic variations of temperature in which 
the temperature is always above normal. 



342 



VETERINARY PATHOLOGY. 



Intermittent fever is the name applied to that type in which 
there are periodic variations, the temperature becoming normal 
between the fever periods. Intermittent fever is observed in 
equine pernicious anemia. 

Fever may also be classified as: 1st. Sthenic. 2nd. As- 
thenic. Sthenic fever is active, vigorous and destructive. As- 
thenic fever has an insidious onset and is slow in action. 





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Fig. 190. — Continuous fever chart showing- morning and evening variations, but a continuous 

high temperature. 

Symptoms. — Fever is usually ushered in by a chill because 
of the constriction of cutaneous vessels which thus diminishes 
the temperature of the skin and produces the sensation of chill- 
ing. There are diminished secretions, as perspiration, saliva and 
urine. In long continued fever there is constipation because of 
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Increased and its character is changed because of the action of 
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ture. 



Lesions. — All parenchymatous structures are affected with 
cloudy swelling, the extent of which depends upon the degree 
of temperature and its duration. Hemolysis is more or less ex- 
tensive. Chronic or long continued fever usually causes hyaline 
degeneration, especially of the vessel walls. The affected animal 
rapidly diminishes in weight because of the consumption of fat. 



CHAPTER XII. 
INFECTIVE GRANULOMATA. 

Infective granulomata embraces a group of specific inflam- 
matory conditions characterized by the proliferation of endothe- 
lial cells, fibroblasts and other cells. Though the consideration 
of the following diseases belongs more properly to a discussion 
of infective diseases, their description will be of value to the stu- 
dent of general pathology. 

TUBERCULOSIS. 

Tuberculosis is a specific, infective disease, caused by the 
bacterium of tuberculosis affecting practically all of the higher 
animals and also some of the lower forms of animal kind. 

Extent. — McFarland states that 14% of the deaths in the hu- 
man family are from tuberculosis. It is probable that 25% of 
all humans have or have had tuberculosis. 

The prevalence of animal tuberculosis is variable in dift'erent 
communities, the percentage depending upon methods employed 
for control and eradication under different sanitary laws, upon 
transportation rules and regulations and upon the conditions un- 
der which the animals are maintained. The exact percentage of 
tubercular animals in any country is not known, but the relative 
number has been determined by tuberculin testing and by post- 
mortem examination at abattoirs. In the United States the 
percentage, generally speaking, is low in comparison with other 
countries. According to the post-mortem findings of 7,621,717 
cattle slaughtered in United States establishments having official 
inspection during the fiscal year beginning July 1st, 1906, and 
ending June 30th, 1907, 29,835, i. e., .4% were tubercular. 
This percentage is probably below the actual percentage, as 
dairy cattle are more extensively affected than beef cattle. The 
Secretary of Agriculture in his report for 1908 holds that 1% 
of beef cattle and 10% of dairy cattle are tuberculous. 

According to the above report 2% is the estimated prevalence 
in the United States of tuberculosis among swine. 

Porcine tuberculosis is apparently on the increase in the 
United States. In Germany it varies from 1-7%. Equine tuber- 

344 



INFECTIVE GRANULOMATA. 345 

culosis is not common in the United States, or at least only a 
few cases have been reported. Tuberculosis is usually found in 
those horses and mules that have been fed on tubercular cows' 
milk. . . 

Tuberculosis of sheep is very rare and the disease is still 
less common in goats. 

Dog and cat tuberculosis is not uncommon and is usually 
observed in pets of tubercular humans, although barn cats, espe- 
cially those fed milk from- tubercular cows, frequently become 
tubercular. (A dairy was recently inspected in which 68% of 
the cows were tubercular and on autopsy three barn cats also 
were found to be affected in a like manner.) 

Tuberculosis of fowls is more prevalent in the United States 




Fig. 193. — Bacterium Tuberculosis Bovine. Pus showing leucocytes and tissue 

shreds. 

than is ordinarily suspected, although the percentage of affected 
birds is difficult of determination because there is at present no 
official inspection of fowls. 

Etiology — Tuberculosis is caused by the Bacterium tuberculo- 
sis. This bacterium has rounded ends and is frequently slightly 
bjent. It varies from 2 to 5 microns in length and from .3 to .5 
in width. (These bacteria may appear as long, delicate, mycelial 
threads, branching forms, or even as a ray like fungoid growth, 
the form depending upon the environment. The pleomorphism 
of this micro-organism has caused some doubt as to its classifica- 
tion as a bacterium.) The Bacterium tuberculosis may occur 
singlv or in pairs, and it is not uncommon to find several lying 



346 VETERINARY PATHOLOGY. 

side by side. They do not form spores, but they may contain 
granules and vacuoles, and they may have a beaded appearance 
because of fragmentation of their cytoplasm. 

The Bacterium tuberculosis is extremely resistant to external 
injurious influences, probably because of a wax-like substance 
that constitutes about one-third of the body weight and forms 
the principal part of the external covering or capsule. (These 
bacteria are stained with difficulty but when once stained retain 
their stain even though subjected to the action of alcohol and 
acids.) The staining peculiarities are probably due to a fatty 
substance they contain. 

Source of infection. — The bacterium tuberculosis may be 
transmitted direct from tubercular to healthy animals, but infec- 
tion is more frequently obtained from foodstuffs, or barns, feed 
racks, watering troughs, posts, soil, eta Tubercular animals 
are almost constantly eliminating the bacterium which contam- 
inates everything that the tubercular discharges contact. The 
cadavers of tuberculous animals are usually deposited in the soil, 
and, in many instances, the proper precautions are not taken to 
destroy the infecting micro-organism. Infected manure is 
spread upon the soil and thus it becomes infected. The various 
crops, including hay, grown upon a tubercular infected soil, may 
be contaminated with the Bacterium tuberculosis and infect sus- 
ceptible animals that consume such food. Sometimes the car- 
casses of animals dead of tuberculosis are thrown into rivers or 
creeks, thus infecting the water. The waste products of many 
small slaughter houses are fed to hogs and this affords oppor- 
tunity for them to become infected. Skimmed milk and whey 
from creameries and cheese factories are also sources of tuber- 
cular infection. 

Channel or avenue of entrance of the infection. — The Bacter- 
ium tuberculosis may gain entrance into the tissues of a healthy, 
susceptible animal through the mucous membranes or through 
abrasions of the skin, though the latter mode of infection is not 
of common occurrence in domestic animals. Cutaneous infec- 
tion is occasionally observed in the mammae of sows and in the 
castration wounds of barrows. 

From clinical and experimental evidence and autopsy lesions 
observed in abattoirs, it seems evident that the digestive tract 
is the principal channel of entrance of the Bacterium tubercu- 
losis in hogs, cattle and fowls. It was originally erroneously 
concluded that the presence of pulmonary tubercular lesions was 
positive evidence that the infection had gained entrance through 
the respiratory tract. Tubercular free experimental animals fed 



INFECTIVE GRANULOMATA. 347 

foodstuff contaminated with the Bacterium tuberculosis have 
frequently become affected w^ith primary pulmonary tubercular 
lesions. (The possibility of inhalation of the infection was care- 
fully guarded against in these experiments.) It is presumed that 
the Bacterium tuberculosis is incorporated by leucocytes in the 
digestive tube and that the leucocytes then pass through the 
intestinal wall into the lacteals and thence to the thoracic duct 
to the right heart and on to the lung, the first capillary system 
encountered, where they may lodge and establish tubercular foci. 
No doubt the respiratory tract is the channel of entrance in some 
cases of tuberculosis, but the number of animals infected through 
this channel is very small. 

An occasional case of tuberculosis may be the result of infec- 
tion through the genito-urinary organs. Thus the penis of a 
bull may become infected by serving a cow afflicted with uterine 
or vaginal tuberculosis, and this same bull by copulation may 
infect other cows. Tubercular lesions are occasionally observed 
in the superficial inguinal glands of steers, and this may be the 
result of infection in the castration wounds. 

Conjunctival infection may occur as a result of forcible dis- 
charge of infection from the respiratory tube of an affected 
animal. 

In summarizing, the digestive, respiratory, cutaneous abra- 
sions, and genito-urinary organs are the principal channels of 
entrance of the Bacterium tuberculosis, the frequency being in 
the order mentioned. 

Lesions. — The characteristic lesion of tuberculosis is the 
tubercle. A tubercle is a nonvascular nodule, composed of leu- 
cocytes, endothelial, giant and connective tissue cells, with a 
tendency for the central part of the nodule to undergo necrosis. 
The lesion may vary in animals of different genera and in differ- 
ent animals of the same genus. Thus tubercular lesions in hogs 
may differ in some particular from those in cattle because of 
variations in the resistance of the hog and ox. Variations of the 
tubercular lesions in different individuals of the same genus occur 
because of variation of Individual resistance of the infected ani- 
mal and variation of the virulency of the infecting organisms. 
Tubercular lesions may be modified or obscured by lesions re- 
sulting from secondary infections. The Initial or primary lesion 
may occur In any tissue or organ. Lymphoid tissue, however, is 
more frequently affected than au}^ other. 

The Bacterium tuberculosis and its products are the etiologic 
factors in the formation of a tubercle. The bacterium having 
lodged in a tissue favorable for its growth and development, be- 



348 



VETERINARY PATHOLOGY. 



gins to multiply and to eliminate those products that stimulate 
the surrounding connective tissue and endothelial cells to in- 
crease in number, and, at the same time, exerts a positive chemo- 
tactic action upon leucocytes. If the influence of tne bacterial 
products is exerted upon the connective tissue and' endothelium, 
the resulting tubercle v^ill be composed of connective tissue cells 
and endothelial cells, and if the influence of the bacterial pro- 
ducts is of a chemotactic nature, the tubercle w^ill contain leu- 
cocytes. 

Structurally, a young tubercle consists of a cellular focus in- 
fected with varying numbers of the Bacterium tuberculosis. As 



M^&M 




fo^w 



Fig. 194 
bercl 



Small cellular tubercle; liver, xSOO. Showing small round cells with tu- 
e bacilli scattered here and there, also a few partially destroyed 

hepatic eels. 



INFECTIVE GRANULOMATA. 349 

rtie bacteria multiply the quantity of their products is increased, 
and these stimulate cellular multiplication and accumulation, and 
thus the tubercle grows. The formation of a tubercle constitutes 
a tissue reaction, but there is no vascularization ; that is, no 
new blood vessels are formed, and the existing capillaries in the 
invaded tissues are finally obliterated. A tubercle is, therefore, 
strictly non-vascular, although in the very beginning the affected 
zone may be hyperemic. Cells constituting a tubercle obtain 
nutriment from adjacent tissues by absorption. Tubercles grow 
by multiplication of the peripheral cells, the central cells becom- 
ing degenerated after they have consumed all available nutrition. 
The structure and appearance of a tubercle varies according to 
its age, thus : a tubercle in the very early stages is a cellular mass, 
a little later the central portion of the cellular mass becomes 
necrotic, and at about the same time a median zone, consist- 
ing of bacteria, endothelial, and, in some cases, giant cells, 
becomes evident ; the outer zone is the active zone and is com- 
posed of bacteria, connective tissue cells and leucocytes. As 
the tubercle becomes larger the necrotic zone extends to the 
median and outer zones toward the periphery. Necrosis is 
usually evident in tubercles that have attained the size of a pea. 
The central necrosis is primarily of the coagulation type, but 
the coagulated necrotic tissue may become liquefied, always be- 
comes caseous and usually calcified according to the quantity of 
fluid contained. The calcification may be limited in extent, the 
necrotic tissue containing small calcareous particles that cause 
the necrotic tissue to have a ''gritty feel," or it may be so ex- 
tensive that the tubercle cannot be dissociated except by the use 
of a sledge. Liquefied tubercular necrotic tissue (pus) is yellow- 
ish in color in the ox, dirty white in hogs and yellowish in fowls. 
It is not sticky, although it becomes quite thick and is finally 
caseated.. 

Tubercles may vary in size from a microscopic point to large 
masses. All tubercles are small in the beginning and are usually 
entirely cellular. Small cellular tubercles in which there is no 
necrosis are designated miliary tubercles. Miliary tubercles ap- 
pear as minute, grayish, translucent, pearl-like specks or nodules. 
If all the lesions in an afifected animal are miliary in character, 
the disease is termed miliary tuberculosis. Miliary tuberculosis 
is most common in hogs. 

The appearance of a tubercle changes when central necrosis 
begins. The color of caseous and calcareous tubercles varies 
from a dirty white to a yellow color. The tubercles may or may 
not be encapsulated. The capsule of a tubercular lesion is rela- 



350 



VETERINARY PATHOLOGY. 



tively thin, though it is tough. Secondary tubercles may develop 
from a primary tubercle, and daughter tubercles may develop 
from a secondary tubercle, thus are produced the irregular nodu- 
lar tubercular masses. The tissues contiguous to a tubercle are 
ischemic, probably because of the enfringement of the affected 
areas with lymphoid cells. ' 

Little difference is noted in tubercular lesions in the various 



c--^ 



Q- 




..a 



Fig. 195. — A Lesion of Tuberculosis from the Post-pharyngeal L,ymph Gland of an 

Ox. A — giant-cells; b — caseous center within tlie tubercle; c — fibrous capsule. 

tissues except possibly osseous tissue and serous membranes. 
Tubercular lesions of osseous tissue are usually associated with 
extensive suppuration of the osseous structures, while tubercular 
lesions of serous membranes are frequently entirely cellular in 
structure and do not undergo central necrosis. 

Boinne tubercular lesions are usually encapsulated and become 
quite extensively calcified. The age of the lesions is sometimes 
important in medico-legal cases. Calcification usually begins 



INFECTIVE GRANULOMATA. 



351 



when the tubercle is from six to eight months of age and is ex- 
tensive by the time the lesion is one year old. Tubercular masses 
are occasionally observed in the lung, bronchial or mediastinal 
glands, and in the liver. These masses may contain all stages of 
tubercular formation or the entire mass may all be in the same 
stage of development, as liquefying necrosis, caseation or calcifi- 
cation. Tuberculosis of serous membranes of bovines should 
receive special mention because of the characteristic appearance 
of the lesions. Bovine serous membrane lesions vary in size from 
a millet seed to a walnut, but are usually about the size of a pea. 
These lesions are frequently thickly studded over large areas of 
a serous membrane. The nodules are surrounded by a firm cap- 
sule which causes them to appear as pearl-like bodies, and hence 




Fig. 196. — Photograph of a tubercular mammary gland, Ox. 



the name, ''pearly disease." Sometimes serous membrane tuber- 
cular lesions are very extensive ; this type m^ay be called "mass 
tuberculosis." 

Porcine Tubercular lesions are characterized by enlargement of 
lymphatic glands, the formation of tubercles of variable sizes in 
or upon serous membranes and within the substance of glandular 
organs, bones and other connective tissues. The tubercles pro- 
duce increased density of invaded soft tissues and are, therefore, 
easily detected except in very recent infection. The tubercular 
nodules in the early stages present about the same color as tlie 
surface of the tissue invaded. In sectioning the tubercle the cen- 
tral portion is caseous and slightly yellow or fibrous and white. 



352 VETERINARY PATHOLOGY. 

Sometimes there is a combination of both conditions and occa- 
sionally the tubercles contain calcareous granules. The central 
portion of porcine tubercles rarely contains liquefied necrotic 
tissue." 

Microscopically porcine tubercular lesions are always cellular 
in the beginning. The cellular tubercles are fairly constant in 
structure regardless of the tissue in which they occur. The 
center is at first represented bv a mass of lymphoid cells, the 
other cellular elements occurring as the tubercle develops. 

Necrosis, or fibrosis^ succeeds the cellular stage in the por- 
cine tubercular lesion. Necrosis of tubercles is probably the 
result of the activity of very virulent bacteria or the low resis- 
tance, of the infected animal. The necrotic center may be sur- 
rounded by a cellular zone (lymphoid and endothelial cells), or 
it may be surrounded by fibroblasts. The necrotic material is 
invariably caseated and later becomes calcified. 

Fibrous lesions vary from the formation of small quantities 
of fibrous tissue to dense fibrous centers. Fibrous lesions are 
probably produced by bacteria of low virulence, or occur in ani- 
mals having a marked resistance. The central portion of the 
fibrous lesion mav become calcified. 

The so-called arbor vitae gland is a fibrous center in which 
the fibrous tissue is arranged siiriilar to the trunk and branches 
of a tree, hence the name. This lesion is observed in the hog 
in the cervical lymph nodes. The bacterium tuberculosis has 
been demonstrated in about 30 per cent of arbor vitae glands. 

The lesions of porcine tuberculosis are in brief either cellu- 
lar, necrotic and calcified tubercles, or cellular, fibrous and calci- 
fied tubercles. The lesion is always non-vascular as in other 
animals. 

Auian tubercular lesions are very similar to mammalian tubercles, 
and may occur in practically any tissue. Microscopically, avian 
tubercules are found to contain giant cells, endothelioid cells, 
small round cells and connective tissue cells, the arrangement of 
whTch is the same as described in mammalian tubercles. Avian 
tubercular lesions have been found in the liver, spleen, intestine, 
mesentery, kidney, lung, skin, and bones, the frequency being 
in the order mentioned. 

Avian tubercles in glandular tissue, i. e., in the liver, kidney, 
spleen, etc., begin as small, dirty, white cellular foci. They usu- 
ally occur singly, though they may occasionally become conflu- 
ent, thus producing nodules a quarter of an inch in diameter. 
As the tubercles in glandular tissue undergo necrosis, they as- 
sume a yellowish color. Intestinal tubercles are about the same 



INFECTIVE GRANULOMATA. 353 

size as those in glandular tissue. The intestinal lesions are usu- 
ally quite hard and dense and present a glistening appearance. 
Necrosis frequently destroys the intestinal wall and thus a tuber- 
cular intestinal ulcer is produced. Mesenteric tubercles are fre- 
quently pedunculated and they invariably present a pearl like 
appearance. 

Extension. — Tuberculosis, except in some cases of the acute 
form, essentially a localized disease. However, the disease, 
even in the chronic form, has a tendency to extend and involve 
new tissue. The extension may be accomplished by means of, 
first, the lymphatic system, second, the digestive, respiratory 
and genito-urinary tubes, third, the blood vascular system and 
fourth, by continuity and contiguity. 

Tuberculosis is usuall)^ extended by the lymphatic circulation. 
Thus the first group of lymph nodes through which the lymph 
passes from a tubercular lesion is almost invariably involved. In 
fact this is a characteristic of the disease. The large per cent of 
lymphatic lesions is also evidence of extension by means of the 
lymph. It has been previously stated that hogs are invariably 
infected by ingestion of tubercular material and in 93 per cent of 
tubercular hogs the submaxillary lymph nodes are aflected, which 
is further evidence of lymphatic extension. The fact that infec- 
tion may extend along the digestive, respiratory or genito-urin- 
ary tracts, has been demonstrated. Thus the discharges, con- 
taining the Bacterium tuberculosis from a pharyngeal tubercle 
m.ay pass through the oesophagus and stomach and find a nidus 
favorable for its development in the intestine. In a like manner 
the lung tissue may become affected by extension from laryngeal, 
tracheal or bronchial tuberculosis and prostatic tuberculosis may 
result from extension of renal tubercular lesions. In extensive 
or generalized tuberculosis the tubercles not infrequently in- 
volve and produce necrosis of the blood vessel walls and the 
virulently contaminated necrotic material being discharged into 
the blood resulting in tubercular metastasis. Thus tuberculosis 
is extended bv means of the blood. Extension by the blood in- 
variably results in generalized tuberculosis which is usually 
acute. 

In the discussion of tubercular lesions, the formation of sec- 
ondary and daughter tubercles was mentioned. The production 
of secondary and daughter tubercles is a means of extension. 
If the newly formed tubercles are in the same kind of tissue as 
the primary tubercle then the extension is by continuity. If the 
secondarv or dausfhter tubercles are in tissues dissimilar to that 



354 VETERINARY PATHOLOGY. 

in which the primary tubercle occurs the extension is by con- 
tiguity. 

In the majority of the cases of lymphatic extension and in 
some of the cases of blood extension the Bacterium tuberculosis 
is incorporated in and transported by leucocytes. The leucocytes 
usually have sufficient vitality to destroy the incorporated bac- 
teria but occasionally the leucocytes may be destroyed after 
having transported the bacteria a considerable distance. Thus a 
Bacterium tuberculosis from a pulmonary tubercle may be incor- 
porated by a leucocyte and carried to the kidney and the leuco- 
cyte being destroyed the liberated bacterium may establish a tub- 
ercular focus in the renal tissue. The occurrence of Bacterium tub- 
erculosis in the milk of cows having no mammary tubercular 
lesions as well as the fact that ingestion of tubercular material 
frequently causes pulmonary tuberculosis, may be due to leuco- 
cytic incorporation and transportation of the infecting micro- 
organism. 

Elimination. — From the sanitary point of view it is alw'ays of 
considerable importance to know the channels or avenues 
through which infectious agents are discharged in order that they 
may be destroyed. Tuberculosis affects all tissues and the Bac- 
terium tuberculosis may not be eliminated from the affected ani- 
mal or it may be discharged in one or more of the secretins or 
excretions. It has been determined by the Department of Agri- 
culture that about 40 per cent of tubercular cattle eliminate the 
Bacterium tuberculosis in their feces. The same investigators 
also found, in a lim.ited number of dairies, that about 25 per 
cent of tubercular cows, regardless of location of the lesions, 
eliminated the Bacterium tuberculosis in their milk. These are 
facts of prime importance in adopting means for checking the 
progress or for suppression of the disease. The discharges from 
the respiratory tract of tubercular animals frequently contain the 
Bacterium tuberculosis, especially if they have pulmonary lesions 
of the disease. The urine and discharges from the female genital 
organs may be contaminated with the infection. Renal tuber- 
culosis, however, is not of frequent occurrence and it is not 
probable that the Bacterium tuberculosis is eliminated in the 
urine of tubercular animals in which there are no renal lesions. 

In general the channel of elimination of the bacterium tuber- 
culosis depends largely upon the location of the lesion. 

Tuberculin and Tuberculin Test. — Tuberculin is a bio-chemic 
material containing the products and the disintegrated bodies 
of the Bacterium tuberculosis. It is prepared by growing the 
Bacterium tuberculosis in glycerine bouillon for a certain length 



INFECTIVE GRANULOMATA. 355 

of time. The glycerine bouillon culture is filtered and the fil- 
trate sterilized by heat and concentrated to the desired strength 
by evaporation over a water-bath. The active principle of tuber- 
culin is probably a nucleo-proteid or its chemic derivatives. 

Tuberculin is a very reliable diagnostic agent. Its chief use 
in veterinary medicine has been in the diagnosis of tuberculosis 
in cattle. It is practically as reliable in the detection of human, 
porcine and probably avian tuberculosis as in the detection of 
bovine tuberculosis. The principal method of application has 
been by subcutaneous injections and noting the temperature 
changes in the suspected animal. The normal temperature of the 
animal is ascertained previous to the injection and the tempera- 
ture is taken every two hours, beginning eight hours after tuber- 
culination. On the day succeeding the injection a rise of from two 
to three degrees Fahrenheit is considered a reaction and this sig- 
nifies that the patient is tuberculous. This reaction is probably 
due to the specific irritating action of the injected tuberculin 
upon the tubercular foci producing intense hyperemia around 
and disintegration of the tubercle. Thus there is a sudden dis- 
charge of tubercular products into the system and the intense re- 
action, thermic and constitutional follows. 

A purified tuberculin used directly in the conjunctival sac 
is now on the market. The ophthalmic reaction consists of the 
production of a marked hyperemia of the conjunctive in from 
six to ten hours after tuberculination. At the present time 
the technique is at fault or the tuberculin is of inferior quality 
and the ophthalmic tuberculin test cannot be relied upon. 

ACTINOMYCOSIS. 

Actinomycosis is a specific, inflammatory granuloma, caused 
by the Cladothrix actinomyces and characterized by the forma- 
tion of tumorous masses of fibrous tissue that usually develop 
suppurating centers and fistulous tracts. 

Distribution and extent. — Actinomycosis is prevalent in Eu- 
rope, Australia, Africa, North and South America. The extent 
of the disease varies in different countries. According to the 24th 
Annual Report of the Bureau of Animal Industry there were 
slaughtered in establishments having federal inspection 7,621,717 
cattle, of which 22,742 were found to be affected with actinomy- 
cosis, or one in about each 340. The actual per cent is even 
larger, for many animals afflicted with actinomycosis are slaugh- 
tered where there is no official inspection maintained. 

Susceptible Animals. — Cattle are more frequently affected 



356 



VETERINARY PATHOLOGY. 



with this disease than other animals, though actinomycosis of 
sheep, goats and hogs is occasionally reported. A few cases 
have also been observed in the horse, mule, dog and wild ani- 
mals. 

Etiology. — A fungus, the Cladothrix actinomyces or actino- 
myces bovis, is the specific cause of actinomycosis. The life his- 
tory of this organism is not known, but it is thought that it 
passes a part of its life cycle upon some of the grasses. Each 
matured fungus is composed of a central body 10 to 40 microns 
in diameter, from which the radiating filaments (mycelia) extend 
outward for a distance of from 5 to 20 microns, then becoming 
enlarged, terminate in club-shaped bodies from 10 to 50 microns 
in length. Thus the matured fungus has the appearance of a 
rosette and is commonly called the "ray fungus." Detached clubs 
are capable of reproducing the entire rosettes as described. The 
fungus can be cultivated in artificial media where it develops 
a tangled mass of mycelia. 

Source. — The Cladothrix actinomyces is probably most fre- 




f-ah^.^ 



Fig. 197. — Drawing of Actinomyces (Ray fungus) in section of tongue. 



INFECTIVE GRANULGMATA. 357 

quently obtained from vegetation, especially wild rye (Hor- 
dinm murinum) consumed bv the animal. Infection occurs most 
frequently in animals fed on dry feed as fodder, stover, straw or 
hay. During January and February, 1908 .86% or 376 cattle of 
41,405 slaughtered had actinomycosis of the tongue or submax- 
illary lymph nodes, and of 12,484 cattle slaughtered in July, 1908, 
44 or .34% were affected with actinomycosis. Some rather exten- 
sive outbreaks have been investigated in which it seems highly 
probable that infection has been direct from one animal to an- 
other, or indirect by means of the discharge of actinomycotic ani- 
mals that had been smeared on rubbing posts, feed racks and feed 
troughs. (Of 98 head of cattle, three of which were actinomycotic 
when placed in the feed lot in November, 42 head were affected 
with actinomycosis when inspected 2^ months later.) 

Channel of Entrance. — The causative fungus may gain en- 
trance into the system by way of the digestive tract, the respira- 
tory tract or through the skin. Abraded surfaces appear to be 
essential for infection, though it has not been proven that the 
fungus cannot penetrate uninjured surfaces. The digestive tract 
is the most frequent channel of entrance in cattle. The tongue, 
especially the dorsal surface at the junction of the base and apex, 
is subject to injury by the rough, harsh food consumed by cattle. 
Tongue injuries may also be inflicted by licking boards, posts, 
etc., containing nails and splinters. Awns of wheat, barlev and 
rye, chafif, splinters and hair accumulate in the erosions or wounds 
of the tongue, producing the so-called ''hair sores." More than 
12% of 48,000 cattle slaughtered during the winter months in one 
of the Kansas City packing houses had "hair sores" upon their 
tongues. The "hair sore" is intimately associated w4th lingual 
actinomycosis ; indeed it is rare to find actinomycosis of the 
tongue or submaxillary lymph glands when there is no "hair 
sore." Diseased teeth, especially if the gingival mucous mem- 
brane is involved, also provide an entry for the ray fungus. The 
possibility of the infection passing^ through the intestinal or 
gastric wall explains the cases of peritoneal actinomycosis that 
are occasionallv observed 

Respiratory infection is not of common occurrence. This type 
of infection probably occurs by inhalation of chaff or awns con- 
taminated with the Cladothrix actinomyces. 

The skin is probably the most frequent channel of entrance 
in hogs. Actinomycotic scirrhus cords are quite common, the in- 
fection taking place in the castration wound. Mammary acti- 
nomycosis is sometimes observed in sows, especially those run- 
ning in stubble fields, the infection taking place through abra- 



358 VETERINARY PATHOLOGY. 

sions produced by the stubble. Abrasions resulting from rub- 
bing on stanchions and feed boxes may be a source of infection in 
dairy cattle. 

Lesions. — Macroscopic. — Actinomycotic lesions may be sur- 
face or subsurface. The fungus may invade and produce the 
lesion in any tissue. 

Surface lesions begin as small inflammatory centers v^hich 
usually thicken and become elevated above the general surface. 
The lesion gradually increases in size, and in some cases assumes 
a fungoid appearance. At this stage the lesions vary in size from 
a small pea to a walnut. The surface tissue may become eroded 
as a result of the extension of necrosis from the lesion and the 
typical actinomycotic pus discharged or more frequently the 
lesion becomes encapsulated by the formation of a dense fibrous 
capsule. The capsule usually limits the development of the lesion 
and it may be diminished in size by the contraction of the fibrous 
tissue constituting the capsule. 

Subsurface lesions, though beginning as inflammatory centers, 
are invariably Circumscribed by, a dense, fibrous wall. As 
the disease progresses the center of the lesion undergoes lique- 
fying necrosis. The necrosis extends, producing irregular, tor- 
tuous sinuses that may extend through the capsule and into the 
surrounding normal tissue. Ultimately the liquified necrotic 
tissue (pus) would ordinarily be discharged upon a surface, or 
the fungus contained in the necrotic tissue (pus) would perfor- 
ate the primary capsule and cause the production of a secondary 
fibrous capsule. Thus the lesion is frequently composed of sev- 
eral communicating cavities (multilocular) containing actinomy- 
cotic pus. If such a lesion is incised and pressure applied the 
typical beads of actinomycotic pus will appear in various 
places upon the cut surface. Actinomycotic pus is creamy, 
sticky, tenacious, yellowish-white and contains small, yellow, 
gritty granules. The pus has a greasy feel and may have a 
slight odor. If the pus is permanently maintained within the 
capsule, its fluid content is absorbed and becomes caseous. 

Osseous actinomycosis is of common occurrence. The fungus 
having gained entrance produces inflammation, which is suc- 
ceeded by disintegration of the osseous tissue and the formation 
of cavities or pockets. By growth and extension of the infect- 
ing fungus, inflammation and disintegration is favored, and thus 
communicating cavities are formed in the afifected bone. As the 
process of rarefaction continues within there is new osseous tis- 
sue deposited without. Thus bone afifected with actinomycosis 



INFECTIVE GRANULOMATA. 



359 



becomes enlarged and cancellous and has a honeycomibed ap- 
pearance. 

Microscopic. — The presence of the Cladothrix actinomyces in 
a tissue produces an irritation resulting in an accumulation oi 




o 

s 

•o 

a 

c 



o 
p. 



^ 



360 VETERINARY PATHOLOGY. 

small round cells, the production of endotheloid and giant cells by 
the invaded tissue, and finally the development of a fibrous cap- 
sule around the entire mass. The fungus may appear in the be- 
ginning as mycelial elements, but later it has the typical rayed 
appearance. In old lesions the central portion or body of the 
fungus becomes calcified. "^ 

Surrounding the clubs or mycelium in the early stages are 
varying numbers of small, round cells (lymphocytes). 

As the disease progresses, the matured fungus is more or 
less surrounded by giant cells that actually contact the fungus. 
The actinomycotic giant cell is very irregular in shape and size 
and has varying numbers of nuclei scattered indiscriminately 
throughout the cell body. 

Endotheloid cells appear marginally to the giant cells. These 
cells are similar in appearance to the endotheloid cell of tuber- 
culosis, having a relatively large cell body and a small, single 
nucleus. 

The small, round cells are first noticed immediately around 
the fungus, but later they infiltrate the surrounding tissue also, 
and are in excess of all other cells in the lesion. 

Fibroblasts appear in the margin of the early lesion, and 
through their activity a thick fibrous capsule is produced. 

Actinomycotic pus is found to be composed of tissue shreds 
and fragments, lymphoid cells and some polymorphonuclear 
leucocytes, an occasional endotheloid cell and the Cladothrix 
actinomyces. 

Extension. — The extension of actinomycosis has usually been 
described as taking place only by growth in continuity or contig- 
uity, or by passing along the respiratory, digestive or genito- 
urinary tubes. By a careful observation of over 72,000 cattle 
slaughtered, it has been found that many cases, in which there 
were "hair sores" but no actinomycotic tongue lesions, showed 
actinomycosis of the submaxillary lymph nodes. The majority 
of cases of lingual actinomycosis are accompanied bv involve- 
ment of the submaxillary lymph nodes. That practically all 
cases of actinomycosis of the submaxillary lymph nodes occurred 
in animals having ''hair sores'' is indicative of lymphatic exten- 
sion. It is therefore quite probable that actinomycosis may be 
extended in the animal body by means of the lymph. 

Differential Diagnosis. — Bovine actinomycosis may be con- 
founded with tuberculosis, nodular disease, abscess formation 
and various tumors. 

Tubercular lesions calcify, actinomycotic lesions rarely be- 
come calcified. Tubercular,, pus is usually quite different from 



INFECTIVE GRANULOMATA. 361 

actinomycotic pus. The former is not sticky or tenacious, and 
does not contain the small, yellow, gritty granules found 
in the latter. The capsule of an actinomycotic growth is 
thicker and denser than the capsule of a tubercular growth. The 
two diseases can be differentiated positively by microscopic ex- 
amination of the pus and the lesion. The Bacterium of tuber- 
culosis would be found in tubercular pus and the Cladothrix 
actinomyces in the actinomycotic pus. Tubercular lesions are 
characterized by the presence of the horse shoe giant cell, the 
actinomycotic giant cell is irregular in outline and size, is poly- 
nuclear, the nuclei being scattered indiscriminately through the 
the cell body. 

Nodular disease, though not very prevalent in cattle may be 
mistaken for actinomycosis. The nodules of nodular disease 
are in the intestinal wall. The pus in the nodule is greenish yel- 
low in color, and though fluid in the early stages, it later be- 
comes caseous but never contains the calcareous granules. 
Microscopically the finding of the Cladothrix actinomyces in 
actinomycotic lesions or pus and the absence of this fungus in 
the lesions of nodular disease is sufficient for differentiation. 

From abscesses the differentiation may be made by the pecul- 
iarity of the pus, and the capsule, which is usually much more 
dense in actinomycotic lesions than in abscesses. 

Osteosarcomata may produce lesions in bone similar to actin- 
omycotic lesions. A microscopic examination is always suffi- 
cient for differentiation of these diseases. 

Ovine actinomycosis may be confounded with ovine caseous 
lymphadenitis and nodular disease. Ovine caseous lymphaden- 
itis is essentially a disease of lymphoid tissue characterized by 
the formation of greenish yellow pus that later caseates in con- 
centric layers, but never contains gritty granules. The color of 
the pus and the arrangement of the caseated necrotic tissue is 
usually sufficient for differentiation of ovine caseous lymphaden- 
itis from actinomycosis. 

The remarks on the differentiation of nodular disease in 
bovines is equally applicable to ovines. 

GLANDERS. 

Glanders is a specific, infective disease, especially affecting 
equines, caused by the bacterium mallei. 

Glanders is prevalent in all countries with the possible ex- 
ception of Iceland, Australia, and some isolated islands. The 
disease is found in practically all parts of the United States. It is 



362 VETERINARY PATHOLOGY. 

more prevalent in those portions of a country in which there is 
extensive horse traffic. The invasion of a province or a country 
by an army is usually succeeded by the appearance of glanders. 

Etiology. — Glanders is caused by the Bacterium mallei. This 
organism was described by several different investigators in 
1882. It is similar in appearance to the Bacterium tuberculosis, 
has rounded ends, is from 2 to 3.5 microns in length and .3 to 
.5 microns in width. This bacterium occurs singly except that 
w^hen grown upon potato medium, pairs or even long filaments 
are not rare. Like, the Bacterium tuberculosis, it produces ple- 
omorphic forms when cultivated in different media or under 
varying conditions. In old cultures it frequently becomes 
short and is sometime coccoid in appearance. Branching forms 
are not uncommon. It does not form spores. ' 

The Bacterium mallei is stained by aqueous solutions of ana- 




Fig. 199. — Bacterium Mallie, xlOOO. 

line dyes that are slightly alkaline in reaction, such as Loef- 
fler's methylene blue. It is so-called "Gram negative," i. e., 
it is decolorized by Gram's solution. 

Source of Infection. — Infection probably occurs most fre- 
fluently in an indirect manner, i. e., the infection is obtained 
from some surrounding object or thing that has been contamin- 
ated with the infected discharges of a glandered animal. 

The Bacterium mallei is strictly parasitic and the source of 
the micro-organism is either the discharges from an infected 
animal or the carcasses of animals that have died of 
glanders. Fortunately this bacterium possesses little re- 



INFECTIVE GRANULOMATA, 363 

sistance to light, dessication and other external influ- 
ences and consequently the infection in discharges is as a rule, 
promptly destroyed. The length of time that the Bacterium 
mallei may exist outside of the animal body and retain its viru- 
lency has never been absolutely determined. Authentic cases 
of glanders have appeared in horses that had been placed in 
stalls that had been vacant for one year, but prior to that time 
occupied by glanderous horses. A few reports are indicative of 
the fact that the Bacterium mallei may retain its virulence in 
infected buildings for two or even three years, but these re- 
ports need further substantiation. It seems probable from clin- 
ical and experimental evidence that, except in the animal body, 
the virulence of Bacterium mallei is rarely retained longer than 
one year. 

In cities, public drinking fountains, hitching posts and feeding 
troughs are probably the greatest sources of infection. The 
purchase of second hand harness, wagons, and other equipment 
should be regulated by ordinances or laws to prevent the 
spread of such infections as glanders. 

The Channels of Entrance of the Infection. — All exposed 
surfaces and natural openings of the body may permit the Bac- 
terium mallei to gain entrance to the tissues. In glanders, as 
in tuberculosis it has been quite conclusively demonstrated 
experimentally that the majority of the cases of glanders results 
from the ingestion of the Bacterium mallei. No doubt infection 
may occur by inhalation of the infectious agent and an occa- 
sional case may be the result of cutaneous inoculation. It is 
possible for the discharges containing the Bacterium mallei to 
become pulverized and carried by air currents and in- 
haled. Farcy may or may not result from cutaneous infec- 
tion. Such inoculations are easily accomplished by bridles, 
harness, saddles, curry combs, etc. More rarely the conjunc- 
tival membrane may be the channel of entrance. For example 
a horse, affected with nasal glanders mav sneeze or cough and 
thus infection be forcibly introduced onto the mucous mem- 
brane of the eye of another horse. 

Lesions. — Macroscopic. — The lesions of glanders are found 
especially in the mucous membrane of the anterior respiratory 
passages, lymph nodes, lung and skin, the frequency being in 
the order mentioned. It is probable that the Bacterium mallei 
primarily affects lymphoid tissue. The gross lesions may be 
diffuse or circumscribed, depending upon the virulency of the 
infecting organisms and the resistance of the affected animal.. 

Diffuse glander lesions are usually found in animals having* 



364 VETERINARY PATHOLOGY. 

little resistance and in which the disease assumes an acute 
form. In the nasal mucous membrane, diffuse, glanderous les- 
ions appear as severe inflammation in which the submucosa is 
extensively infiltrated. The engorgement of the tissue may be 
sufficient to obstruct circulation and result in necrosis of the 
mucous membrane thus producing ulcers variable in size and ir- 
regular in contour. The submaxillary lymph nodes are invari- 
ably hard and enlarged and may or may not be adherent to the 
maxilla. 

Pulmonary, diffuse glander lesions vary in size from a hazel 
nut to a basket ball and are irregular in shape. These lesions 
are grayish or dirty white in color. The lesions may undergo 
a central necrosis or they may become fibrous in nature. The 
necrotic material may be of a semi-solid or caseous consis- 
tency and in the smaller foci there may be calcification. In 
practically lall cases of pulmonary glanders the bronchial and 
mediastinal lymph nodes are enlarged and contain cellular necro- 
tic or fibrous centers. 

Diffuse cutaneous lesions are not of com.mon occurrence. 
They may be present in acute general glanders, the manifesta- 
tion in the skin being of the nature of a diffuse gangrenous der- 
matitis. Cutaneous nodular lesions may become diffuse as a 
result of rapid and extensive necrosis. Difl'use lesions occur 
in lymphoid tissue. Splenic lesions are usually nodular though 
a few cases have been reported in which there were dift'use 
lesions of the spleen. Osseous lesions are usually diffuse and 
appear as a suppurative osteitis. 

Nodular lesions are common in animals that have a marked 
resistance or in those cases infected with mildly virulent bac- 
teria. In chronic glanders the lesions are usually nodular. 

The appearance of nodular lesions in the nasal, pharjmgeal 
and tracheal mucous membranes as well as in the mucous lin- 
ing of the facial sinus varies according to the age of the lesion. 
In the beginning the lymphoid tissue of the mucosa or submu- 
cosa becomes swollen and the tumefaction is surrounded by a 
hyperemic zone. As the disease progresses there is necrosis 
which not only involves the lesion but also the surface tissue, 
thus producing an ulcer. The size depth and contour of the 
ulcer necessarily depend upon the extent of the necrosis. In 
some instances the nasal septum and facial bones may be per- 
forated. The ulcers vary in size from mere points to areas as 
large as a silver dollar. The large ulcers are usually the result 
of two or more necrotic centers becomingr confluent. The de- 
nuded surface is usually limited or surrounded by a raised 



INFECTIVE GRANULOMATA. 



365 



border, the latter being the result of cellular infiltration. The 
tissue adjacent to the denuded surface may finally produce 
sufficient new tissue or granulation tissue to repair the injury. 
If the necrosis involves only the superficial epithelium the re- 
pair will be complete and there will be no scar, but if the 
necrosis has involved the mucosa and portions of the submucosa. 



D, 



A 





A. 
1. 



3. 
B. 
1. 

2. 
3. 



Fig. 200. — Xasal septa, showing glanderous ulcers. 
A nasal septum from glandered horse. 
A crateriform ulcer having a thick raised border with a depressed granulating 

center. 
Shows characteristic outline of an ulcer, also fusion of two or more 

primary ulcers. 
Thumb tacks. 

A nasal septum from a second glandered horse. 
Typical crateriform ulcers and large necrotic area the result of fusion of several 

ulcers. 
Cicatrices shown as irregular white spots. 
Thumb tacks. 



Z66 



VETERINARY PATHOLOGY. 



there will be large quantities of cicatricial tissue produced and 
cpnsequently a scar. In nodular glanders of the anterior air 
passages, the submaxillary lymph nodes are invariably enlarged 
and contain fibrous, caseous or calcified necrotic foci. 

Pulmonary nodular lesions are usually dirty white in coU.r 
and vary in size from pin point centers to masses as large as a 
man's head. These nodules in the beginning are entirely cellu- 
lar and are surrounded by an hyperemic zone. As they become 
larger the central portion usually becomes necrotic and tlie 
hyperemic zone becomes infiltrated with fibroblasts that pro- 
duce a fibrous capsule. The small nodular lesions may be small 
and thickly distributed throughout the entire lung. The large 




Fig. 201 — Cutaneous Glanders — Faro.v. 

i. A large erosion or ulcer (farcy bud) on the internal surface of fetlock. 
2, 3 and 4. Other ulcers appearing along the course of the lymphatics. 



INFECTIVE GRANULOMATA. 



367 



lesions are usually few in number and they may be fonneci by 
two or more nodules becoming confluent. The central casecus 
necrotic tissue in the small foci frequently becomes calcified. 
Calcification is usually not evident in the large pulmonary les- 
ions. The bronchial and mediastinal glands are invariably in- 
volved and they may be caseous, calcified or indurated. 

Nodular lesions of the skin are found in the superficial por- 
tion of the dermis or in the subcutaneous tissue. The nodules 
in the skin rarely become larger than a pea but those of the 
subcutaneous tissue may become as large as a hen's egg. The 
central portion of the cutaneous and subcutaneous nodules and 




^■:i->j-*r,,-:y>^<^^-' 



X 



fit 



Fig. 202 — Microscopic Section through a glanderous ulcer. 

1. Margin of ulcer-necrotic tissue. 

2. Normal nasal mucous membrane. 
2. Showing- depth of erosion. 

4. Small round cells. 

5. Epitheloid cells. 

6. Fibrous tissue. 



the superficial tissue covering them become necrotic and a 
sticky, tenacious, semi-fluid material is discharged onto the 
surface. The related lymphatic vessels are all engorged and 
the lymph nodes are enlarged and later become indurated. 

The tissue destroyed in the lesions of cutaneous ghmders 
may be partially regenerated, but are more frequently repaired 
by the substitution of fibrous tissue thus producing a thickened 
fibrous skin. 

Small nodular lesions have been noted in the spleen, liver 
and kidney. The splenic lesions may be caseous or calcified. 
Hepatic lesions are usually caseous. The portal lymph nodes 
are usuallv involved when lesions are present in the liver and 



368 VETERINARY PATHOLOGY. 

the lymph nodes along the hilus of the spleen are invaded in 
splenic lesions. 

Microscopic. — A small lesion is the result of a diffuse prolif- 
eration of lymphoid and endotheloid cells and migration of 
polymorph leucocytes. The proliferated cells may accumulate in 
groups, thus producing nodules. In the beginning there is usu- 
ally a well marked hyperemic zone around the cellular center 
The cells constituting the central portion of the lesion later un- 
dergo necrosis and about the same time the hyperemic zone 
becomes less evident. A fibrous capsule may or may not en- 
close the lesion, depending upon v^hether it is diffuse or nodular. 

In the nodular form of the disease there is a proliferation of 
fibroblasts in the tissue that was previously hyperemic. The 
fibroblasts produce the capsule that characterizes nodular gland- 
ers. In the older subsurface centers there is formed caseous 
material and in the small centers calcareous particles. In sur- 
face lesions, necrosis or fibrosis is evident. 

Diagnosis. — Mailein is a filtrate obtained from a glycerinated 
bouillon culture of the Bacterium mallei. Mallein is of diagnostic 
value only. The cause of the reaction of glandered horses to mallein 
is due to increased tissue action. The reaction noted in glanders con- 
sists in a thermic disturbance, a swelling at the point of inocu- 
lation, stiffness in gait, general depression and there is usually 
frequent urination. The temperature variations in glanders range 
from 2° F. to 5° F. The maximum rise of temperature usually 
occurs in from ten to twelve hours after malleination, though it 
may not appear until the eighteenth hour after injection of the 
mallein. The high temperature evidenced in a mallein reaction 
is maintained for a period of from 24 to 60 hours. The swelling 
is usually quite large and is very sensitive. The lymphatic ves- 
sels that are related to the swollen area become engorged and 
present a knotted appearancee. The swelling characterizing a 
mallein reaction persists for several days. Stiffness of gait may 
be due largely to the disturbance induced by the swelling at 
the point of injection, but at least in some cases it is evident that 
the stift'ness of gait is not proportional to the size of the swell- 
ing. Aside from stiffness the reacting animal has a dejected 
appearance. The cause of frequent urination is not known. 

Agglutination. — The bacterium mallei produces an agglutinogen 
which causes the animal body to produce an agglutinin. A spe- 
cific agglutinin is found in small quantities in the blood serum 
of normal horses and in larger quantities in horses with gland- 
ers. The agglutination test for glanders depends upon the 
same principle, as that upon which the typhoid agglutination 



INFECTIVE GRANULOMATA. 369 

depends. The agglutinin appears to cause the bacterial cell 
membrane to become sticky and thus the bacteria acted upon 
tadhere to each other when they are brought into contact and 
clumps or clumping of the bacteria results ; this constitutes 
the agglutination reaction. Blood serum is obtained from the 
suspected animal and placed in a normal salt solution in which 
are suspended dead Bacteria mallei. A series of four tubes is 
usually used in order that different dilutions may be made. In 
the 1st tube the dilution is made 1 to 200, i. e. one part of serum 
is taken to 200 parts of salt solution in which the Bacterium 
mallei is suspended. In the 2nd tube, the dilution is made 1 to 
500, the 3rd tube 1 to 800 and in the 4th tube, 1 to 1200. These 
tubes are placed in an incubator. The reaction consists in a 
deposit of clumped or agglutinated Bacteria mallei in the bot- 
tom of the tube. Normal horse serum usually contains suffi- 
cient agglutinin to produce a reaction in tube number one, that 
is in a dilution of 1 to 200. A deposition in tube number two is 
considered suspicious and deposits in tubes three and four is 
positive evidence of glanders. The reaction time is from 21: 
to 60 hours. 

The agglutination test is an accurate means of diagnosis it 
the test fluid is properly prepared and has been properly pre- 
served and if the operator uses care in making the test. The 
time required is much less than the time necessary in making 
the mallein test. Another advantage is that the blood serum of 
an animal dead of suspected glanders can be as readily tested as 
the serum from a living animal — hence it is useful in medico- 
legal cases. 

EPITHELIOMA CONTAGIOSUM. 

Epithelioma Contagiosum is a specific infective disease of 
fowls and it may be transmissible to pigeons. The disease is 
widespread in the United States, It is, according to Gary the 
most serious drawback to the poultry industry of the south. It 
is quite prevalent in Hawaii, and has been described in many 
different localities in Europe. 

Etiology. — The cause of contagious epithelioma is unknown. 
The evidence obtainable at the present time indicates that the 
eiologic factor is either a protozoon, (coccidium), or an ultra 
microscopic or filterable virus. 

Lesions. — Macroscopic. — ^The disease is initiated by a catarrhal 
inflammation of the mucous membrane of the head and neck. 
The disturbance may be localized in the eye, nose or mouth, or 



370 



VETERINARY PATHOLOGY. 



may involve all those parts. The inflammatory disturbance stim- 
ulates or is accompanied by a proliferation of epithelial cells in 
the eye, nose, mouth or even on the wattles and comb. These 
epithelial new growths are at first grayish, have a smooth, glis- 
tening appearance and are surrounded by a hyperaemic zone. 
Later the growths, which become nodular, undergo degenera- 
tion, especially upon the surface. The necrotic tissue may re- 
main and form a scab or it may slough leaving a ragged, brown- 




Fig. 203. 
Left side of head, showing eye with extensive accumulation of caseous necrotic 

material. 



ish or grayish indurated surface. These nodules may become 
as large as la pigeon's Qgg. They frequently entirely obstruct 
vision and in some cases destroy the eye ; those appearing in 
the nostril may seriously interfere with respiration or even 
obstruct the air passages ; and nodules in the buccal cavity may 
prevent eating or the prehension of food ; while those that occur 
in or upon the wattles and comb may be so extensive that 
these structures are practically destroyed. These nodules may 
entirely undergo necrosis, the necrotic tissue becoming dry 
and scaly or necrosis may begin in the center of the 
nodule and be of a liquefying character and when the entire 
nodule has undergone necrosis the mass is discharged as a 
thick, watery fluid containing flakes of coagulated necrotic tis- 
sue. Again the discharge may be thick and creamy or it may even 
be of a caseous nature. 



INFECTIVE GRANULOMATA. 



371 



Microscopic. — These nodules are found to be composed largely 
of epithelial cells supported by irregular bands of connective 
tissue in which there is a limited blood supply. The majority of 
cells are very large. Some of these cells contain oval re- 
fractile bodies that have been considered as protozoa by some. 







Fig. 204. 
Right side, showing growth from eye, nasal cleft, and mouth. 



These bodies are also observed betw^een the cells. The epithelial 
cells, especially those in the center of the nodule, usually show 
more or less of a nuclear disintegration. The marginal cells in 
the nodules are usually more or less flattened. The cell nests 



372 



VETERINARY PATHOLOGY. 



may develop from glandular or surface epithelium, v^hich, in 
the attempt to repair the eroded surface, becomes entangled in 
the ragged edges of the ulcers and develop as an epithelioma. 

The cell nests increase in size by a multiplication of the peri- 
pheral epithelial cells. The rapidly multiplying marginal cells 




Fig. 205. — Microscopic section of Epithelioma contagiosum. 

1. Surface of growth from nasal mucous membrane. 

2. Area of epithelial cells, cells large in center, becoming smaller and finally 

blending with the connective tissue. 
o. Apparently connective tissue undergoing mucoid degeneration. 

4. Probably blood vessels, but the cells are smaller than normal red blood cells 

of the chicken. The cells are also quite irregular in shape. 

5. Degeneration of central cells. The nucleus of the cell first degenerates and 

finally the cell body. 



consume practically all of the central cells and there is central 
necrosis of the cell nests. 

The nests are irregular in size and outline and they are 
grouped to form the nodules. The nodules may or may not 
have bands of clear, hyaline substance that represents fibrous 
tissue undergoing hyaline or mucoid degeneration. 



GLOSSARY. 



Ablated (L.Ab, from and Ferre, to bear). 
Removal of a part as by cutting off. 

Abnormalities (L.Ab, from and Norma, 
rule). Conditions not in accord with 
the usual. 

Aborted (L.Ab, from and Oriri, to arise). 
Prevented from full development. 

Abraded (L.Ab, from and Radere, to 
rub). Having the surface tissue 
rubbed off. 

(ibscess (L-Ab. from and Ceder, to de- 
part). A circumscribed, molecular 
disintegration of sub-surface tissue- 
Absorption (L.Ab, from and Sorbere, to 
suck in). The process of taking up 
substances into the tissues. 

Accessory (L. Accessorius, additional). 
In addition to. 

Achromatosis (Gr.A, without, Chroma, 
color and osis, a condition of). A 
condition of absence of color. 

Acidophile (L.Acere, to be sour and Gr. 
Phileein, to love). Readily stain- 
able with acid dyes. 

Acini (L. Acinus, a grape). The small- 
est lobules or parts of a compound 
structure. 

Acromegaly (Gr.Okros, end and Megalos, 
large). A condition characterized by 
overgrowth of the extremities and 
face. 

Actinomycosis (Gr.Aktis, a ray, Mukes, 
fungus and osis, a condition og). A 
disease caused by the "ray fungus." 
Cladothrix actinomyces. 

Adenoma (Gr.Aden, gland and Oma, 
tumor). An epithelial tumor re- 
sembling a gland in structure. 

Adipocere (L.Adeps, fat and Cera, wax). 
A wax-like substance formed by 
exposure of tissue of a cadaver to 
moisture with air excluded. 

Aerobic (Gr.Aer, air and Bios, life). 
Requiring free oxygen (air) in or- 
der to live and multiply. 

Agglutinin (L.Agglutinare, to stick to- 
gether). An adaptation product oH 
the body cells produced by immu- 
nization with corresponding cells 
which causes a clumping or coales- 
cing of the kinds of cells used In 
immunization. 

Agglutinogen (L Agglutinare, to stick 
together). A substance present in 

373 



bacterial immunization which gives 
rise to the production of agglutin- 
ins by the body cells. 

Alveolar (L.Alveolus, a small lobe). 
Pertaining to an alveolus, (A small 
cavity for a tooth or histologic di- 
vision in a lung, gland, etc.) 

Amboceptor (Gr.Ambo, both and L. Ca- 
pere, to take). One of the types oC 
receptors or intermediary bodies Ira 
Ehrlich's lateral side-chain theory- 

Amitosig (Gr.A, without and Mitos, 
thread.) Direct division of cells 
without formation of thread-like 
structures. 

Amniotic (Gr.Amnion. a foetal mem- 
brane.) Pertaining to the amnion, 
one of the foetal membranes. 

Amoeba (Gr.Amoibe, a change.) A co- 
lorless, single-celled, animal organ- 
ism that constantly undergoes 
changes of form. 

Amylaceous (Gr. Amnion, starch.) Of 
the nature of, or containing starch. 

Amylin (Gr. Amnios, starch.) The In- 
soluble wall of a starch grain. 
Starch cellulose. 

Amyloid (Gr.Amulos, starch and Eidos, 
form.) Like starch. 

Anabolism (Gr.Ana, up and Ballein, to 
throw.) The transformation of food- 
stuffs into complex tissue-elements. 

Anaerobic (Gr.A, without, Aer, air and 
Bios, life.) Able to live in the ab- 
sence of free oxygen or air. 

Anaphase (Gr.Ana, up and Phasfs; 
phase.) The third stage in mitotic 
cell division. 

Anasarca (Gr.Ana, up and Sarx, flesh.. 
An accumulation of non-inflamma- 
tory serum in the sub-cutaneous 
areolar tissue. 

^astomosis (Gr.Ana up and Stomoein, 
to bring to a mouth.) The establish- 
ment of a communication between 
two distinct portions of the same 
organ (Usually vessels). 

Anemia (Gr.A, without and Haima, 
blood.) A deficiency of blood or of 
any of its constituents 

Angioblast (Gr.Aggeion, a vessel and 
Blastos, germ.) One of the cells of 
angioblastic origin concerned in the 
formation of vessels 



374 



GLOSSARY. 



Angioma (Gr.Aggeion, vessel and Oma, 
tumor.) A tumor composed of ves- 
sels independently of pre-existing 
blood or lymph vessels. 

Anhydremia (Gr.A, without, Hudor, wa- 
ter and Haima, blood.) A diminu- 
tion of the watery constituents of 
the blood. 

Ankylosis (Gr.Agkulos, stiffened, and 
osis, a condition of.) A union of 
bones in an articulation. 

Anlagen (Ger.Anlagen.) The founda- 
tion or design of a structure, the 
beginning. 

\noniaIy (Gr.A, without and Homalos, 
average.) A marked deviation from 
the normal. 

Antenatal (L.Ante, before and Natus, 
born.) Existing before birth. 

Anthracosis (Gr.Anthrax, black and 
osis, a condition of.) A lung disease 
characterized by deposition of coal 
dust. 

Antitoxin (Gr.Anti, against and Toxi- 
kon, poison.) A substance elabo- 
rated by the body-cells to counter- 
act the toxins of other cells. 

Aplasia (Gr.A, without and Plasis. for- 
mation.) A condition of failure of 
development. 

Apnoea (Gr.A, without and Pheein, to 
breathe.) A transient cessation of 
respiration. 

Argyriasis (L.Argentum, silver and osis, 
a condition of.) A condition of pig- 
mentation by deposition of silver. 

Arteriolith (Gr.Arteria, to keep air, 
trachea and Lithos, stone.) A cal- 
culus or stone in an artery. 

Arteriosclerosis (Gr.Arteria, trachea, 
Skleros, hard and osis. a condition 
of.) A chronic inflammation of ar- 
teries with hardening of the walls, 
especially of the intlma. 

Arthropoda (Gr.Arthron, a joint and 
Pous, foot.) A class of animals hav- 
ing jointed legs. 

Ascites (Gr.Askos, a bag.) An abnor- 
mal collection of non-inflammatory 
fluid in the peritoneal cavity. 

Assimilation (L.Ad. to and Similare, to 
make like*) The process of taking up 
food-stuffs by the tissues and mak- 
ing them a part of themselves. 

Asthenic (Gr.A, without and Sthenos, 
strength.) Characterized by absence 
of strength or violence. 

Asymmetrical (Gr.A, without, Sun, to- 
gether and Metron, measure.) Be- 
ing unlike in corresponding organs 
or parts of opposite sides of a body 
that are normally of the same size. 

Atavismal (Gr.Atavus, grandfather.) A 
condition of reappearance in an in- 



dividual of a peculiarity possessed 
by a more or less remote progeni- 
tor. 

Atelectasis (Gr.A, without, Telos, form 
and Ektasis, expansion.) Imperfect 
expansion or collapse of the air ves- 
icles of the lung. 

Atheromatous (Gr.Athere, gruel, Oma, 
tumor and ous, of the nature of.) 
Of the nature of an aethroma. (A 
sebaceous cyst containing a grumous 
material.) 

Atresia (Gr.A, without and Tretos, per- 
forated.) Failure of a normal open- 
ing or canal to develop. 

Atrophy (Gr.A, without and Trophe, 
nourishment.) A condition in which 
there is a decrease in size or num- 
ber of the composing cells of an 
organ or tissue. 

Atypical (Gr.A, without and Tupos, 
type.) Not conforming to type. Ir- 
regular. 

Autosite (Gr. Autos, self and Sitos, food.) 
A monster capable of independent 
existence after birth. 

Avidae (L.Avis, bird.) A family of ver- 
tebrates. 

Bactericidal (Gr.Bakterion, a little stick 
and L.Coedere, to kill.) Destructive 
to bacteria. 

Basophile (Gr.Basis, foundation and 
Pheleein, to love.) A substance that 
readily combines with basic dyes. 

Benign (L.Benignus, kind.) Not danger- 
ous to health or life. 

Bifida (L.Bis, twice and Findere, to 
cleave.) Divided into two parts.) 

Biologic (Gr.Bios. life and Logos, stu- 
dy.) Pertaining to Biology. (The 
study of the structure, function and 
organization of living forms.) 

Buccal (L.Bucca. cheek.) Pertainmg to 
the cheeks. 

Bursattae (L. Bursa, purse.) Small bur- 
sae or vessels. A disease of the skin 
characterized by necrosis. 

Calcified (L.Calx, lime and Fiere, to be- 
come.) A condition of deposition of 
calcareous matter in tissues. 

Canalization (L.Canalis, a canal.) The 
process of formation of canals. 

Caries (D.Caries, rotten.) The molecular 
necrosis of bone, enamel, dentine, 
etc. corresponding to necrosis in 
soft tissue. 

("arcinoma (Gr.Karkinos, crab and Oma, 
tumor.) A malignant epithelial 
newgrowth. 

Catarrh (Gr.Katarrhein. to flow down.) 
An inflammatory condition of a 
mucous membrane in which there Is 
an excessive production of mucus. 

Caustic (Gr.Kaiein, to burn.) A sub- 



GLOSSARY 



Z7d 



stance that destroys tissue. More 
violent than corrosive. 

Cellulose (L.Cellula, a small cell and 
osis, a condition of.) The principal 
constituent of cell-membranes. 

Cementum (L,.Caementum, a rough 
stone.) A plastic material capable 
of becoming hard and of binding 
together contiguous materials. 

Centrosome (Gr.Kentron, center and 
Soma, body. J A structural part of 
a cell in active mitotic cell-divi- 
sion. 

Ceruminous (L.Cera, wax and osis, a 
condition of.) Of the nature of cer- 
umen. (The wax of the ear.) 

Chalicosis (Gr.Chalix, gravel and osis, 
a condition of.) A disease of the 
lungs caused by the inhalataion of 
dust. 

Chemotaxis (Gr.Chemia, chemistry and 
Tassein, to arrange.) The property 
of cell attraction or repulsion due 
to chemic substances. 

Chlamydo (Ger.Chemus, a cloak.) A 

cloak or mantle. (Used as a limit- 
ing prefix.) 

Cholelithiasis (Gr.Chole, bile, Lithos, 
stone and osis. a condition of.) The 
condition in which there are cal- 
culi in the gall-bladder or ducts. 

Cholesteatoma (Gr.Chole, bile, Stear, 
fat and Oma, tumor.) A tumor 
composed of pearl-like masses of 
epithelial tissue mingled with 
more or less cholesterin. 

Choroid (Gr.Chorion, chorion and Eidos, 
like.) The vascular tunic of the eye 
continuous with iris and between 
the sclerotic coat and retina. 

Chromatin (Gr.Chroma, color.) The part 
of the protoplasm of a cell that 
takes up stains. 

Chromatolysis (Gr.Chroma, color and 
Luein, to loose.) The destruction of 
coloring matter. 

Chromosome (Gr.Chroma, color and 
Soma, body.) One of the minute 
bodies into which the chromatin of 
the cell is resolved in indirect cell- 
division (Mitosis. J 

Cicatricial (L. Cicatrix, a scar.) Of or 
pertaining to a cicatrix. 

Cicatri.x (L. Cicatrix, scar.) The con- 
nective tissue that replaces a local 
loss of tissue. 

Circumscribed (L.Circum, around and 
Scribere to write.) Of limited or 
defined extent. 

Cirrhosis (Gr. Kirrhos, reddish-yellow.) 
An overgrowth of connective tissue 
in an organ usually the result of 
chronic inflammation. 

Cirsoid (Gr.Kirsos, a varix and Eidos, 



form ) Resembling a varix. (A di- 
lated and tortuous vessel. 

Clonic CGr.Klonos, commotion.) Char- 
acterized by spasmodic and convuls- 
ive muscular contractions alternat- 
ing with relaxations. 

Clot (A.S.Clate, a burr.) A special soli- 
dification of the blood outside of a 
vessel. 

Coagulated (L.Coagulare, to curdle.) A 
condition in which "here is a coag- 
ulum. 

Coagulum (Coagulare, to curdle.) a 
solidification of the blood occurring' 
in a dead vessel. 

Coagulation (L. Coagulare, to curdle.) 
The process of forming a coagu- 
lum. ) 

Coalesce TL.Coalescere, to grow to- 
gether.) The union of two or more 
parts of things. 

Coccidiosis (Gr.Kokkos, a berry and 
osis, a condition of. j The condition 
of being affected with Coccidia, a 
genus of unicellular protozoa. 

Collagen (Gr.Kolla, glue and Gennaein, 
to produce, j A substance of the 
body, especially of cartilage, that is 
converted into a gelatin by boiling. 

Collagenous (Gr.Kolla, glue and Gen- 
naein, to produce.) of the nature 
of Collagen. 

Collateral (L.Con, together and Latus 
side.) Of the nature of an acces- 
sory, not direct. 

Colliquation (L.Con, together and Li- 
quare, to melt.) The liquefaction 
or breaking down of a tissue or 
organ. 

Coma (Gr.Koma, a deep sleep.) A 
state of unconsciousness not influ- 
enced by external stimuli, control 
of vital functions still persisting. 

Compensatory (L.Compensare, to equal- 
ize.) Restoring a balance or defi- 
ciency of a part by means of some 
other part or organ. 

Complement (L.Cum, together and Pie- 
re, to fill.) That which supplies a 
deficiency. 

Complex (L.Cum, together and Plere, 
to fill.) The totality of a thing. A 
thing taken as a whole with consi- 
deration of its make-up of parts. 

Component (L.Cum, together and Po- 
nere, to place, j One of the parts 
that make up a body. 

Concentric (L. Cum, together and Cen- 
trum, center.) Arranged in an 
equidistant manner about a common 
point. 

Congenital (L.Cum, together and Gr. 
Gennaein, to produce.) Existing for 
occuring at birth. 



376 



GLOSSARY. 



Cungrestion (L.Con, together and Ce- 
rere, to bring.) An abnormal col- 
lection and retention of blood in 
the vessels of a part. 

Conglomerate (L.Cum, together and 
Glomerare, to heap up.) Arranged 
in a mass together indiscriminately. 

Conidia (Gr.Konis, dust and diminutive 
term.) The deciduous, axial spores 
of certain fungi. 

Conjuiration (L.Cum, together and Ju- 
gare, to yoke.) A condition of being 
joined. 

Contiguity (L.Cum, together and Tan- 
gere, to touch.) A condition of being 
in contact. (Spoken of two different 
kinds of tissue.) 

Continuity (L. Cum, together and Ti- 
gere, to touch.) A condition of being 
without interruption of part. 

(Within the same tissue.) 

Conventiogially (L.Con, together and,'Ve- 
nire, to come.) According to agree- 
ment. 

Comified (L.Cornu. horn and Facere, to 
make.) The condition of having 
been made or having become horny. 

Corporation (L. Corpus, a body.) A col- 
lective body considered as one or 
taken as a whole. 

Corpuscle (L. Corpus, body and diminu- 
tive term.) A small body or struc- 
ture. Usually the cell-content of the 
blood. 

Correlated (L. Con, together and Rela- 
tio, relation.) Related to. 

Corrosive (L.Con, together and Rodere, 
to gnaw.) A substance that destroys 
tissue (less violent than a caustic). 

Cortical (L. Cortex, bark.) Of or per- 
taining to the cortex, the surface 
layer. 

Cotyledons (Gr.Kotuledon, a socket.) 
An enlarged vascular organ of the 
chorion. 

Croupous (A.S.Kropan, to cry aloud.) 
Of the nature of croup. Character- 
ized by a development of a mem- 
branous deposit or exudate on the 
surface of a mucous membrane. 

Cutaneous (L. Cutis, skin.) Pertaining 
to the skin. 

Cycle (Gr.Kuklos, a circle.) A round of 
years. A period of time. 

Cystadenoma (Gr.Kustis, bladder, Aden, 
giand and Oma, tumor.) An aden- 
oma containing cysts. 

Cystic (Gr.Kustis, a bladder.) Pertain- 
ing to or resembling a cyst. 

Cytoplasm (Gr.Kutos, cell and Plessein, 
to mold.) The essential, viscid sub- 
stance of a living cell. — Proto- 
plasm. 



Cytosis (Gr.Kutos, cell and osis. a con- 
dition of.) Cell proliferation. 

Death (A. S. Death.) The total cessation 
of life. 

Debris (L.Dis, apart and Briser. to 
break.) The material resulting from 
the destruction of anything. 

Decubital (L.Decubitus, a lying down.) 
The position of lying down. 

Degeneration (L.De, away from and 
Gerere, to become.) A morbid con- 
version of the elements of a tissue 
into new substance. 

Deleterius (L.Delere, to destroy.) Char- 
acterized by a hurtful or destruc- 
tive tendency. 

Denticle (L.Dens, tooth and diminutive 
term.) A small tooth or projecting 
point. 

Depleted (L.De. from and Plere. to 
fill.) Condition of diminished amount 
of fluid in a body or part. 

Dermatologic (Gr. Derma, skin and Lo- 
gos, study.) Pertaining to derma- 
tology. The study of the skin. 

Dessicant (L.Dessicare, to dry up.) A 
substance that has the property of 
drying up other substances. 

Dessicated (L.Dessicare, to dry up.) A 
condition of being dried up. 

Detritus (L.De, away from and Terere, 
to rub.) Finely divided material worn 
off from substances by rubbing. 

Diabrosis (Gr.Dia, through and Bibros- 
kein, to eat.) A condition of having 
been broken through corrosive ac- 
tion. 

Diapedesis (Gr.Dia, through and Pedae- 
in, to leap.) The passage of blood 
through an unruptured vessel-wall. 

Diaster (Gr.Dis. two and Aster, star.) 
The so-called double star or wreath 
in the mittoic cell division. 

Diastole (Gr.Dia, through and Stole, a 
drawing.) The period of dilatation 
of the chamber of the heart. 

Dichotomous (Gr.Dicha, asunder and 
Temnein, to cut.) Regularly divid- 
ing into pairs from bottom to top. 

Diffuse (L.Dis, apart and Fundere, to 
pour,) Not limited in extent. 

Digestion (L.Dis, apart and Gerere, to 
carry.) The preparation of food- 
stuffs for absorption and assimila- 
tion. 

Diphtheritic (Gr. Diphtheria, skin or 
membrane.) Pei-taining to diphthe- 
ria, or characterized by formation 
of false membrane in and upon a 
mucous membrane. 

Disintegrated (L.Dis. apart and Integer, 

a whole.) Broken up or decomposed. 

Dissimilation (L.Dis, apart and Simu- 



GLOSSARY. 



377 



lare, to make like.) To cause to ap- 
pear different. 
Dissociated (L.Dis, apart and Sociare, to 
associate.) A condition of being se- 
parated or broken up. 
Dropsy (Gr.Hudrops, dropsy.) The col- 
lection and retention of a- non-in- 
flammatory lymph transudate within 
a tissue or body-cavity. 
Eburnated (L.Ebur, ivory.) An increased 

density of bone, similiar to ivory. 

Ecchymosis (Gr.Ek. out and Chumoma, 

a flowing- out.) An extravasation of 

blood into the subcutaneous tissues. 

Ectropia (Gr.Ek, out and Trepein, to 

turn.) Eversion or turning out of 

the edge of a part, especially of the 

eyelid. 

Effervescence (L.Efferveacere, to boil 

up.) Giving off bubbles of gas. 
Effusion (L.Effundere, to pour out.) The 
escape of a liquid exudate into a 
tissue or part, especially of serum 
or blood. 
Elimination CL.Ex, out and Limen, 
threshold.) The expulsion of any- 
thing from the body, especially of 
waste products. 
Emaciation (Emaciare, to become lean.) 
A condition resulting from a general 
wasting away of all tissues of the 
body. 
Embolus (Gr.En, in and Ballein, to 
throw.) An obstruction in a vessel 
by matter from another point. 
Embryonal (Gr.En, in and Bruein, to 
grow.) Pertaining to an embryo. The 
foetus in the early stages of its de- 
velopment. 
Emphysema (Gr.Emphusaein, to Inflate.) 
A condition in which there is an 
accumulation of gas in the inter- 
stices of the connective tissue. 
Empyema c Gr.En, in and Puon, pus.) 

Pus in a body cavity. 
Encephaloid (Gr.Egkephalos, brain.) Of 

the nature of brain tissue. 
Endemic (Gr.En, in and Demos, people.) 
A disease found in a certain place 
more or less constantly. 
Endomysium (Gr. Endon, within and 
Mus, muscle.) The connective tissue 
structure separating muscle-flbre 
bundles. 
Endothelium (Gr.Endo, within the Thele 
nipple and Oma, tumor.) A tumor 
composed of endothelial cells. 
Endothelium (Gr.Endo, within and The- 
le, nipple.) Cells covering the inner 
surface of vessels not communicat- 
ing with the outer air. 
Endotoxin (Gr.Endon, within and Toxi- 
kon. poison. ) A poisonous substance 



found within the cell body of a bae- 
terium. 
Enterolith (Gr.Enteron, bowel and Lith- 
os, stone.) A concretion found in 
the intestines: An intestinal calcu- 
lus. 
Enterorrhagia (Gr.Enteron, bowel and 
Hregnunai, to burst forth.) He- 
morrhage into the intestines. 
Enucleated (L.Ex, out of and Nucleus, 
kernel. ) Removed in such a way 
that the body comes out clean and 
whole from its capsule (as of a tu- 
mor.) 
Enzootic (Gr. En, in and Zoon, animal.) 
Pertaining to a disease of lower 
animals and found in a certain place 
more or less constantly. 
Enzym (Gr.En in and Zume, leaven.) 

A ferment formed within the body. 
Enzymotic (Gr.En, in and Zume, leaven.) 

Pertaining to leaven, (Enzym.) 
Eosinophile (Gr.Eos, dawn and Philee- 
in to love.) Showing a peculiar af- 
finity for eosin or acid stains in 
general. 
Ependymal (Gr.Epi, upon and Enduma, 
a garment.) Pertaining to the Epen- 
dyma. The lining membrane of the 
cerebral ventricles and of the cen- 
tral canal. 
Ephemeral (Gr.Epi, upon and Hemera, 
day.) Lasting but a day; tempo- 
rary. 
Epidermal (Gr.Epi, upon and Derma, 
skin'.) Pertaining to the epidermis, 
the outer layer of the skin. 
Epilepsy (Gr.Epi, upon and Lepsis, sei- 
zure.) Paroxysmal loss of conscious- 
ness with convulsions lasting but a 
short time. 
Epistaxis (Gr.Epi, upon and Stazein, to 
cause to drop.) Hemorrhage from 
the nose. 
Epithelium (Gr.Epi, upon and Thele, nip- 
ple.) Cells forming the epidermis 
and lining vessels that communicate 
with the external air. 
Etiology (GrAitios, cause and Logos, 
stud}'. ) The study of the causes of 
disease. 
Evolutionary (L.Ex. out and Volvere, to 
roll.) Pertaining to evolution: The 
process of development from simple 
to complex form. 
Exanthematous (Gr.Ex, out of and Ant- 
hema, a breaking forth and ous 
pertainmg to.) Of the character of 
Exanthema: An eruption of the skin 
Exciting (L.Ex, out and Citare, to stir.) 

Caliini? forth directlj. 

Excrement (L.Ex, out and Cernere, tc 

separate.) Matter cast out as waste 

from the body (especially the feces.) 

Excretion (L. Ex, out and Cernere, t.; 



378 



GLOSSARY. 



separate.) The discharge by the tis- 
sues of waste products. 
Exfoliate (L. Ex, from and Foliare, to 
give forth leaves.) To separate into 
thin layers. 

Exfoliation (L.Ex, from and Foliare, to 
give forth leaves.) The process of 
separating into thin layers. 

Exophthalmic (Gr.Ex, out and Oph- 
thalmos, eye.) Pertaining to abnor- 
mal extrusion of the eye-ball. 

Extirpation (L.Ex, out and Stirps, 
stem.) Complete removal or eradica- 
- -.1 of a |)ari. 

Extravasation (L. Extra, outside, and 
Vas, vessel.) The escape of fluid 
from its containing cavity or ves- 
sel. (Especially applied to the 
blood.) 

Extra-uterine (L>. Extra, outside of and 
Uterus, uterus.) Outside of the ute- 
rus. 

Extrinsic (Extra, without and Secus, 
otherwise.) Coaiir,^- from the out- 
side: Not directly belonging to a 
part. 

Exudate (Ex, out and Sudare, to sweat.) 
A portion of the blood that has 
passed into a tissue from its ves- 
sels because of inflammatory dis- 
turbances. 

Exudation (L.Ex, out and Sudare, to 
sweat.) The production of an exu- 
date. 

Faceted (Fr.Facette, a little face.) Pro- 
vided with many small plane sur- 
faces. 

Facultative (L.Facultas, capability.) 
Capable of assuming a part or con- 
dition (spoken of bacteria.) 

Fever (L.Fibres. ) An abnormally high 
temperature. 

Fibrinopurulent (L.Fibra, fibre and Pus, 
pus.) Composed of fibrin and pus. 

Fibrinous (L.Fibra, fiber.) Of the na- 
ture of or consisting of fibrin. 

Fibroglia (L.Fibra, thread and Glia, 
glue.) The glue-like fibres of som<j 
tumors. 

Filamentous (L.Filum, a thread and 
ous of the nature of.) Like a small 
thread in structure. 

Filaria (L.Filum, a thread.) A genus of 
nematode worms, thread-like, endo- 
parasitic. 

Filum terminale (L.Filum, a thread and 
Terminale, terminal.) The long, 
slender, thread-like termination of 
the spinal cord. 

Flagella (L.Flagella, a whip.) A motile 
whip-like process (usually applied 
to some bacteria). 

Foci (L.Focus, a fire-place.) The prin- 
cipal seats of a disease. 

Foetus (L.Foetus, offspring.) Unborn 



off-spring of viviparous animals in 
later developmental stage. 

Follicle (L.Follis, a bellows and diminu- 
tive term.) A small sac or gland. 
Fractous (L.Frangere, to break.) Apt 
to become difficult to control. 

Fracture (L.Frangere. to break.) A 
break in the continuity of osseous 
tissue (bone.) 

Function (L.Fungi, to perform.) The 
normal action or work of a part. 

Fusiform (L.Fusus. a spindle and For- 
ma, form.) Like a spindle in form. 

Galactopherous (Gr.Gala, milk and Fer- 
ein, to bear.) Producing milk. 

Gangrene (Gr.Gangraina, a sore.) That 
type of nerosis characterized by pu- 
trefaction of the necrotic tissue. 

Gemmation (L. Gemma, bud.) The act 
of budding or reproduction by bud- 
ding. 

Gestation (L.Gestare, to bear.) The 
period from fertilization of the ovum 
to its expulsion from the uterus. 

Glia cells (L.Glia, glue.) Neuroglia or 
the supporting-structure cells of 
nerve-tissue. 

Glioma (Gr.Glia, glue and Oma, tumor.) 
A tumor composed of neuroglia 
cells. 

Glycogen (Gr.GIukos, sweet and Gennaein 
to produce.) A substance formed 
from carbohydrates in the body and 
stored up in certain structures: 
often called animal starch. 

Granulation (L.Granula, a little grain.) 
The formation of new tissue in the 
repair of local loss of tissue and 
composed of capillary vessels en- 
closed by groups of connective tis- 
sue cells. 

Haptophore (Gr.Haptein, to seize and 
Phorein, to carry.) The stable, non- 
poisonous element of a toxin which 
enables it to unite with a antitoxin 
(Ehrlich's lateral side-chain theo- 
ry.) 

Helminths (Gr.Helmins, a worm.) A 
branch of invertebrates known as 
worms. 

Hematemesis (Gr.Haima, blood and 
Emesis, vomiting.) The vomiting 
of blood. Gastric hemorrhage. 

Hematidrosis (Gr.Haima, blood and Hi- 
drosis, sweating.) The sweating of 
blood or of a blood-like substance. 

Hematin (Gr.Haima, blood.) A product 
of decomposition of Hemoglobin. 

Hematocele (Gr.Haima, blood and Kele, 
tumor.) The extravasation of blood 
into a cavity, especially the tunica 
vaginalis testis. 

Hematogenous (Gr.Haima, blood and 



GLOSSARY. 



379 



Gennaein, to produce.) Derived from 
or having origin in the blood. 

Hematoidin (Gr.Haima, blood and El- 
dos, resemblance.) A yellowish- 
brown, iron-free substanice obtained 
from hemoglobin of the blood. 

Hematoma (Gr.Haima, blood and Oma, 
tumor.) A circumscribed collection 
of extravasated blood. 

tiematometra (Gr.Haima, blood and 
Metra, uterus.) An accumulation of 
blood in the uterine cavity, extra- 
vasated from the mucosa. 

Hematuria (Gr.Haima, blood and Ou- 
ron, urine.) Urine containing whole 
blood. A condition of bloody urine. 

Hemochromogen (Gr.Haima, blood, 

Chroma, color and Gennaein, to pro- 
duce.) A crystalline coloring matter 
derived from the hemoglobin of the 
blood. 

Hemocoelia (Gr.Haima, blood and Koi- 
lia, belly.) An accumulation , of blood 
within the peritoneal cavity. 

Hemogrenous (Gr.Haima, blood and Gen- 
naein.) Derived from the blood or 
having origin in the blood. 

Hemoglobin (Gr.Haima, blood and L. 
Globus, globe.) The coloring matter 
of the red blood copuscles. 

Hemoglobinuria (Gr.Haima, blood, L.- 
Globus, a globe and Gr.Ouron, urine.) 
A discharge of urine containing he- 
moglobin. A condition of hemoglo- 
bin in the urine. 

Hemolysis (Gr.Haima, blood and Luein, 
to loose.) Destruction of the blood 
or of its corpuscles. 

Hemoptysis (Gr.Haima, blood and Ptu- 
ein, to spit.) Spitting blood from 
the respiratory passages — pulmonary 
hemorrhage. 

Hemorrhage (Gr.Haima, blood and 
Hragnuni, to burst forth). The es- 
cape of blood through a vessel wall. 

Hemosiderin (Gr.Haima, blood and Si- 
deros, iron.) A golden-yellow pig- 
ment containing iron and' derived 
from the hemoglobin of the blood. 

Hemothorax (Gr.Haima, blood and 
Thorax, thorax.) An accumulation 
of blood in the thoracic cavity. 

Hepatogenous (Gr.Hepa, liver and Gen- 
naein, to produce.) Produced by or 
in the liver. 

Hermaphrodite (Hermes and Aphrodite, 
Greek deities ) An individual that 
possesses more or less completely 
both male and female genital or- 
gans. 

Hernia cGr.Hernos, a sprout.) The pro- 
trusion of an organ through an ab- 
normal opening in the wall of its 
containing cavity. 



Heterogeneous (Gr.Heteros, other and 
Genos, kind.) Composed of different 
substances. 

Humor (L. Humor, moisture.) A fluid or 
semi-fluid part of the body. 

Hyalin (Gr.Hualos, glass.) A translucent 
substance. The chief nitrogen con- 
stitute of hydated cysts. 

Hyaloplasm (Gr.Hualos, glass and Plas- 
sein, to mold.) The fluid portion of 
the cell-protoplasm. 

H;drargyrosis (Gr.Hudor, water and 
Arguros, silver (Mercury.) A deposit 
of mercury in the tissues. 

Hydremia (Gr.Hudor, water and Hai- 
ma, blood.) A condition in which 
the fluid of the blood is in excess of 
the normal proportion of cells. 

Hydrocele (Gr.Hudor, water and Kele, 
tumor.) A collection of oedematous 
fluid within the tunica vaginalis. 

Hydrocephalus (Gr.Hudor, water and 
Kephale, head.) A collection of oede- 
matous fluid in the serous cavities 
of the brain or its meninges. 

Hydropericardium (Gr.Hudor, water. 
Peri, around and Kardia, heart.) A 
collection of oedematous fluid in the 
pericardial sac. 

Hydropic (Gr. Hudrops, dropsy.) Per- 
taining to or affected with dropsy. 

Hydrops (Gr.Hudrops, dropsy.) Dropsy: 
An abnormal collection and reten- 
tion of serum in the cellular tissua 
or in a body cavity. j 

Hydrothorax (Gr.Hudor, water and Tho- 
rax, thorax.) Abnormal accumula- 
tion of an oedematous fluid in the 
pleural cavity. 

Hyperchromatosis (Gr.Huper, above, 
Chroma, color and osis, a condition 
of.) A condition of excessive depo- 
sition of pigment in the tissues. 

Hyperemia (Gr.Huper, above and Hai- 
ma, blood.) An increase in the blood 
supply to a part. 

Hypernephroma (Gr.Huper, above Ne- 
phros, kidney and Oma, tumor.) A 
tumor composed of tissue similar to 
adrenal tissue. 

Hyperplasia (Gr.Huper, above and Plas- 
is, formation.) An increase in the 
number of cells in a part. 

Hyperplastic (Gr.Huper, above and Plas- 
is, formation.) Pertaining to hy- 
perplasia. 

Hypersensitive (Gr.Huper, above and 

L.Sensue, feeling.) A condition of 

increased or abnormal tendency to 
reaction to a stimulus. 

Hypertrophy (Gr.Huper, above and Tro- 
phe, nourishment.) An excessive 



380 



GLOSSARY. 



increase in the size of the cells of a 
tissue. 
Hyphae (Gr.Hupha, a web.) The fila- 
ments composing the mycelium of a 
fungus. 
Hyphomycetes (Gr Hupha, a web and 
Mukes, a fungus.) A group of 
fungi including the molds. Some are 
pathogenic. 
Hypoplasia (Gr.Hupo, under and Plas- 
is, formation.) Defective or incom- 
plete development of a tissue. 
Hypothesis (Gr.Hupo, under and Tithe- 
nai, to put.) A proposition taken 
for granted in order to draw a con- 
clusion to aid in explanation of cer- 
tain facts. 
Ichorous (Gr. Ichor, serum or pus.) Of 
the nature of ichor: An acrid, thin, 
puriform discharge. 
Ichthyosis (Gr.Ichthus, a fish and osis, 
a condition of.) A condition like 
the scales of a fish. 
Icterus (Gr.Ikteros, yellow.) Jaundice, 
a yellow pigmentation of the tis- 
sues with the coloring matter of the 
bile. 
Immunity (L.In, not and Munis, serv- 
ing.) A condition of exemption from 
a disease. 
Impacted (L.In, in and Pingere, to 
drive.) Driven firmly in or dislodged 
with difficulty. 
Inanition (L.Inanis, empty.) A wasting 
of the body from lack of food or 
from inability to assimilate it. 
Inbreeding (A.S. In, and Brodan, to 
nourish. ) The production of off- 
spring by closely related parents. 
Incorporated (L.In, and Corpus, body.) 
Thoroughly united with a body in a 
compact mass. 
Indurated (L.In, and Durus, hard.) 

Rendered hard. 
Inert (L,in, not and Ars, art.) Without 

action. 
Infarct (L.In, in and Farcire, to stuff.) 
A wedge-shaped area (hemorrhagic 
||k or anemic) in an organ produced 
lay obstruction of a terminal vessel. 
"Infection (L.In, in and Facere, to 
make.) The invasion of the body by 
pathogenic micro-parasites and the 
sum-total of the disturbances pro- 
duced by their presence therein. 
Infectious (L. In, into and Facere, to 
make.) Capable of communicating a 
disease. 
Enflammation (L.In, and Flamma, flame.) 
The reaction of a living animal tis- 
sue to an irritant accompanied by 
circulatory disturbances and by de- 
structive or proliferative tissue 
changes. 



Ingrested (L.In, in and Gerere, to bring.) 
Taken into the stomach or alimen- 
tary tract. 
Inherited (L.In, to and Haerere, to 
cleave.) Born to or belonging to by 
birth. 
Inhibitins: (L.In, in and Habere, to 
hold.) Holding in check or hinder- 
ing from doing a thing. 
Inimical (L.In, not and Amicus, friend.) 
Having a hostile tendency. Liable to 
injure. 
Inoculating (L.In, into and Oculus, a 
bud.) The introduction of a virus 
of a disease into a wound or abra- 
sion of the skin. 
Inosculation (L.In, into, and Os, mouth.) 
The joining of blood vessels by di- 
rect communication. 
Insidious (L.Insidioe, ambush.) Coming 

on stealthily or imperceptibly. 
Inspissated (L.In, intensive term and 
Spissare, to thicken.) Thickens by- 
removal of fluid. 
Insusceptibility (L.In, not and Susci- 
pere, to receive.) Not having a lia- 
bility to acquire a disease. 
Intercellular (L. Inter, between and Cel- 
la, cell.) Existing between the cells 
of a tissue. 
Interfunicular (L.Inter, between and 
Funiculus, cord.) Existing between 
the bundles of tissue. 
Intermittent (L.Inter, between and 

Mittere, to send.) Characterized by 
intervals between. 
Interstice (L.Inter, between and Stare, 
to stand.) Spaces between or to 
stand between. 
Interstitial (L.Inter, between and Sis- 
tere, to place.) Pertaining to struc- 
tures between the cells of a part. 
(Stroma.) 
Intracellular (L. Intra, within and Cella, 
cell.) Existing within the cells of 
a tissue. 
Intrinsic (L. Intra, within and Secus, 
otherwise.) Situated entirely within 
or pertaining exclusively to a part. 
Intussusception (L.Intus, within and 
Suscipere, to receive.) A slipping of 
one part of an organ (usually in- 
testine.) into the parts beyond. 
Invagination (L.In, within and Vagina, 
a sheath.) The unsheathing of a tis- 
sue. 
Involucre (L.In, in and Volvere, to 
wrap.) The covering or sheath con- 
taining the sequestrum of necrosed 
bone. 
Irritant (L.Irritare, to excite.) Anything 
that produces an excessive action or 
functioning in a responsive tissue. 



GLOSSARY. 



381 



Ischemia (Gr. Ischein, to check and Hai- 
ma, blood.) A local anemia. 

[schiopagrus (Gr.Ischion, hip and Pa- 
ges, union.) A monster with two 
heads and with bodies united at the 
hips. 

Karyokinesis (Gr.Karuon, nucleus and 
Kinesis, motion.) Indirect cell-divi- 
sion with formation of thread-like 
structures. (Mitosis.) 

Karyolysis (Gr.Karuon, nucleus and 
Luein, to loose.) The morbid de- 
struction of the cell nucleus. 

Katabolism (Gr.Katam, down and Ball- 
ein, to throw.) The transformation of 
complex tissue-elements into simp- 
ler ones in the production of energy. 

Keratitis (Gr.Keras, horn or cornea and 
Itis, inflammation.) Inflammation 
of the cornea. 

Keratosis (Gr.Keras, horn or cornea and 
osis, a condition of.) A disease of 
the skin characterized by an over- 
growth of horny tissue. 

Kinetic (Gr.Kineein, to move.) Pertain- 
ing to motion. 

Keloid (Gr.Kele, a claw and Eidos, 
like.) A raised, cutaneous dense 
overgrowth of white fibrous con- 
nective tissue in a cicatrix, very 
common in the negro. 

Lacerated (L.Lacerare, to tear.) Condi- 
tion of being torn apart leaving 
ragged edges. 

Lacunae (L.Lacuna, a small lake.) 
Small pits or depressions: Hollow 
spaces. 

Laminated (L. Lamina, a plate or scale.) 
Made up of laminae, of thin flat 
plates. 

Lecithin (Gr.Lekithos, the yolk of an 
egg.) A complex nitrogenous sub- 
stance found wi<3£'y distributed in 
the body tissues. 

Leiomyoma (Gr.Leios , smooth Mus, 

muscle and Oma, tumor.) A tumor 
composed of unstriped muscle tis- 
sue. 

Lesion (L.Laesio, to hurt.) A mor- 
bid structural change. 

Leucoderma (Gr.Leukos, white and Der- 
ma, skin.) A condition of abnormal 
whiteness of the skin — Albinism in 
patches. 

Leucomain (Gr.Leukos. white of egg and 
Oma.) A product of metabolism 
of the tissues of the body and nor- 
mally present in them. 

Leucocytosis (Gr.Leukos, white, Kutos, 
cell and osis, a condition of.) An 
increase in the relative number of 
leucocytes in the blood. 



Leucoprotase (Gr.Leukos, white and 
Protos, first.) A ferment. 

Leukemia (Gr.Leukos, white and Hai- 
ma, blood.) A condition in whicb 
there is a proportional increase of 
leucocytes in the blood. 

Lobulate (Gr.Lobus, a lobe and diminu- 
tive term.) Containing small lobes. 

Lumen (L.Lumen, light.) The cavity 
surrounded by walls of a tubular 
vessel. 

Lymph (L.Lympha, water.) That por- 
tion of the blood which passes 
through the capillary walls into the 
perivascular spaces and consists of 
diluted plasma, leucocytes and 
usually waste material. 

Lymphogenous (L.Lympha, water and 
Gr. Gennaein, to produce.) Pro- 

ducing lymph. 

Lymphocyte (L.Lympha, water and Gr.- 
Kutos, cell.) A variety of leucocyte 
found in lymph glands. They are 
small, with very large nucleus. 

Lymphorrhagia (L.Lympha, water and 
Gr.Hragnunai, to burst forth.) The 
flow of lymph from a ruptured 
lymph-vessel. 

Lysin (Gr.Luein, to loose.) A cell pro- 
duct with power of cleavage of 
other cells or substances. 

Lj'sis (Gr.Luein, to loose.) A gradual 
decline. Generally used in combina- 
tion to signify destruction or break- 
ing up. 

Maceration (L.Macerere, to make soft.) 
The softening of a solid by soaking 
in a liquid. 

Macroscopic (Gr. Makros, long and Sko- 
pein, to view.) Visible with the un- 
aided eye or without the use of a 
miscroscope. 

Malformation (L.Malus, bad and For- 
ma, form.) An abnormal develop- 
ment of an organ or part. 

Malign (L.Malus, bad.) Likely to kill. 

Mammalia (L. Mamma, breast.) A class 
of vertebrates that suckle their 
young. 

Margination (L.Marginase, to furnish 
with a border.) The act of furnish- 
ing with a district border. (The 
accumulation of leucocytes on the 
interior of a vessel wall.) 

Mast-cell (Ger. Mast-zellen, food-cell.) 
A large type of leucocytes filled 
with basophilic granules, highly 
stainable. 

Melanin (Gr.Melas, black.) A black pig- 
ment, natural in some tissues, often 
pathologic. 

Melanosis (Gr.Melas, black, osis. a con- 



382 



GLOSSARY. 



dition of.) A condition of abnor- 
mal pigmentation with melanin. 

Metabolism (Gr.Meta, after and Baliein, 
to throw.) The phenomena by which 
foodstuffs are transformed into com- 
plex tissue-elements or complex tis- 
sue-elements are converted into 
simpler ones in the production of 
energy. 

Metamorphosis (Gr.Meta, after and 
Morphoein, to change, and osis, a 
condition of.) A change of shape or 
structure, usually a degeneration. 

Metaphase (Gr. Meta, after and Phasis, 
phase.) The second period in in- 
direct cell-division. (Mitosis.) 

Metaplasia (Gr. Meta, after and Plasis, 
formation.) The conversion of a 
developed or matured tissue into 
another closely related tissue. 

Metastatic (Gr.Meta, after and Stasis, 
halt.) Pertaining to Metastasis, 
The transfer of a disease process 
from one organ to another by means 
of blood or lymph. 

Metrorrhagia (Gr.Metra, uterus and 
Hregnunai, to burst forth.) Hemorr- 
hage from the uterine mucosa, the 
extravasate being almost wholly re- 
tained in the uterus. 

Micron (Gr.Mikros, small.) One one- 
thousandth of a millimeter (1- 
25,000 of an inch). Represented by 
the greek letter mu. 

Microparasite (Gr.Mikros, small, Para, 
beside and Sitos food.) A parasite 
requiring high magnification for ob- 
servation. 

Microphyte (Gr.Mikros, small and Phu- 
ton, plant.) A microscopic plant. 

Microscopic (Gr.Mikros, small and Sko- 
peein, to view.) Not visible with the 
unaided eye. 

Microzoa (Gr.Mikros, small and Zoon 
animal.) A microscopic animal or- 
ganism. 

Micturition (L.Micturire, to urinate.) 
The passage of urine. Staling. 

Miliary (L.Milium, millet.) Consisting 
of small tubercles or nodules of the 
size of millet seed. 

Mitosis (Gr.Mitos, thread and osis, a 
condition of.) Indirect cell-division 
with formation of thread-like struc- 
tures. Karyokinesis. 

Mole (L.Moles, a mass.) A mass formed 
in the uterus by arrested develop- 
ment or degeneration of a foetus. 
Also a Nevus. 

[Monaster (Gr.Monos, single and Aster, 
star.) The single star or wreath in 
indirect cell-division (mitosis). 

Monoohorionic (Gr.Monos, single and 



Chorion, a foetal membrane.) Hav- 
ing a single chorion. 
Mononuclear (Gr.Monos, single and L..- 
Nucleus, nucleus.) Having but one 
nucleus. 
Morbid (L. Morbus, disease.) Pertaining 

to disease. 
Moribund (L.Moriri, to die.) In a dying 

condition. 
Morphology (Gr.Morphe, form and Lo- 
gos, study.) The study of the form 
and structure of organized beings. 
Mucus (L. Mucus.) The viscid fluid se- 
creted by special glands of mucous 
membranes. 
Multiparous (L.Multus, many and Pare- 
re, to produce.) Bringing forth 
more than one offspring at a birth. 
Mycelial (Gr.Mukes, a fungus and He- 
los, an overgrowth.) Pertaining to 
a mycelium. 
Mycelium (Gr.Mukes, a fungus and He- 
los, an overgrowth.) The vegetative 
filaments of a fungus. 
Mycosis (Gr. Mukes, fungus and osis, a 
condition of.) A growth of fungus 
in the tissue. 
Myeloid (Gr.Muelos, marrow and Eidos, 

like.) Resembling marrow. 
Myoblast (Gr.Mus, muscle and Blastos, 
germ.) A cell developing into a 
muscle fibre. 
Myoma (Gr.Mus, muscle and Oma, tu- 
mor.) A tumor composed of muscle 
tissue. 
Myositis (Gr.Mus. muscle and Itis, in- 
flammation.) Inflammation of mus- 
cle tissue. 
Myxodema (Gr.Muxos, mucus and Oide- 
ma, oedema.) A condition in which 
tissues, especially the hands and 
face, are infiltrated with a mucus- 
like substance. 
Myxoma (Gr. Muxos, mucus and Oma, 
tumor.) A connective-tissue tumor 
made up of mucin-containing inter- 
cellular substance. 
Nascent (L.Nanciscor, to arise.) Just 
coming into existence. Just liberated 
from a chemical compound. 
Necrobiosis (Gr.Nekros, a corpse and 
Bios, life.) Gradual and progressive 
death of a cell or of a group of 
cells. 

Necrosis (Gr.Nekros, a corpse.) Death 
of a tissue suddenly, in mass while 
surrounded by living tissue. 

Neoformation (Gr.Neos, new and L. For- 
ma, form.) A circumscribed new 
growth of tissue of abnormal struc- 
ture and location and functionless. 
Tumor. 

Neoplasm (Gr.Neos, new and Plassein, 



GLOSSARY. 



383 



to mold.) A neoformation, a tu- 
mor. 

Neurilemma (Gr. Neuron, nerve and 
Lemma, a husk.) The covering- 
sheath of a nerve-fibre. 

Neuroglia (Gr. Neuron, nerve and Glia, 
glue.) The tissue forming the basis 
of the supporting framework of the 
central nervous tissue. 

Neuroma (Gr. Neuron, nerve and Oma, 
tumor.) A tumor composed of nerve 
tissue. 

Neuter (L.Neuter, neither.) Neither the 
one nor the other. Inactive. Neither 
acid nor alkaline. 

Neutrophile (L.Neuter, neither and Gr. 
Phileein, to love.) A cell or struc- 
ture stainable by neutral dyes. 

Nevus (L. Nevus, a mole.) A mole. A 
congenital angioma of the skin. 
Birthmark. 

Nidus (L. Nidus, a nest.) The original 
point of a morbid process or focus 
of infection. 

Noxious (L.Noxious, harmful.) Having 
harmful properties. 

Nucleolus (L.Nucleus, a small nut and 
diminutive term.) A small body, 
within the nucleus of a cell. 

Nucleoplasm (L.Nucleus, a small nut 
and Gr.Plassein, to mold.) The pro- 
toplasm of a nucleus. 

Nucleus (L.Nucleus. a small nut.) The 
essential part of a living cell. 

Obligatorj' (L.Oblgare, to bind.) Bound 
by conditions. Not facultative. 

Odontoma (Gr.Odons, tooth and Oma, 
tumor.) A tumor of tooth-like 
structure. 

Oedema (Gr.Oidema, a swelling.) The 
accumulation and retention of lymph 
in lymph vessels and spaces. Dropsy. 

Oogenesis (Gr. Oon, egg and Gennaein, 
to produce.) The origin and de- 
velopment of the egg. 

Ophthalmia (Gr.Ophthalmos, the eye.) 
Inflammation of the structures of 
the eye. 

Opsonin (Gr.Opsono, a dainty food.) A 
product of the body-cells that pre- 
pares bacteria for phagocytosis. 

Optimum (L.Optimus, best.) A condi- 
tion characterized by the most fav- 
orable conditions. 

Organized (Gr.Organon, organ.) Con- 
verted into an organ or organ-like 
structure. 

Oscillation (L.Oscillare, to vibrate.) A 
regular motion back and forth 
within narrow limits. 

Osmotic (Gr. Osmos, impulse.) Pertain- 
ing to osmosis. The passage of li- 
quids and substances in solution 
through a membrane. 



Ossification (L.Ossa, bone and Facere, 
to make.) The formation of bone. 

Osteitis (Gr. Osteon, bone and Itis, iji- 
flammation. ) Inflammation of bone. 

Osteoblast (Gr.Osteon, bone and Blas- 
tos, germ.) A cell of mesoblastic 
origin concerned In .the formation 
of bone. 

Osteoclast (Gr.Osteon, bone and Klaein, 
to break.) A large multinuclear cell 
concerned in the removal of bone. 

Osteophyte (Gr.Osteon, bone and Phu- 
ton, plant.) A bony outgrowth, tree- 
like in character. 

otologic (Gr.Ous, ear and Logos, stu- 
dy.) Pertaining to Otology: The stu- 
dy of the ear. 

Oxyphile (Gr.Oxus, sharp and Phileein, 
to love.) Stainable with acid dyes. 

Palpated (L.Palpare, to feel of.) Ex- 
amined with the hand to determine 
conditions beneath. 

Paracentesis (Gr.Para, near and Kente- 
sis, puncture.) Surgical puncture of 
the walls of a cavity. 

Paralysis (Gr.Para, near and Luein, to 
loose.) Loss of sensation or motion 
in a part. 

Parasite (Gr.Para, near and Sitos, food.) 
An organism that gains protection 
or sustenance or both at the ex- 
pense of another organism. 

Parenchyma (Gr.Para, near En, in and 
Cheem, foundation, to pour in.) The 
foundation, or essential or function- 
ing portion of a structure. 

Parenchymatous (Gr.Para, near En, ia 
and Cheem, foundation, to pour in.) 
Pertaining to or affecting the paren- 
chyma. 

Parietes (L. Paries, wall.) The envelop- 
ing or investing structure of a body 
cavity. 

Parturition (L.Parturire, to bring forth.) 
The act of giving birth to young. 

Pathogenesis (Gr. Pathos, suffering and 
Gennaein, to produce.) The origin of 
disease. 

Pathology (Gr. Pathos, suffering and 
Logos, study.) The study of dis- 
ease. 

Peptons (Gr.Pepton, digesting.) Pro- 
teids formed by the action of pep- 
sin on albumins during digestion. 

Perichondrium (Gr.Peri, around and 
Chondros, cartilage.) The fibrous 
connective-tissue covering of carti- 
lage. 

Perimysium (Gr.Peri around and Mus, 
muscle.) The sheath of connective- 
tissue around a fasciculus of mus- 
cle fibres. 



384 



GLOSSARY. 



Periostoid (Peri, around. Osteon, bone 
and oid, of the nature of.) Of the 
nature of periosteum: The sheath 
of connective tissue around bones 
excepting on articular surfaces. 

Peripheral (Gr.Peri, around and Ther- 
ein, to carry.) Pertaining to the pe- 
riphery: The external boundary. 

Petrification (Gr.Petra, a stone and L.- 
Facere, to make.) Conversion into 
a stone-lilie substance. 

Phagocytic (Gr.Phagein, to eat and Ku- 
tos, cell.) Pertaining to a phago- 
cyte. 

Phagocytosis (Gr.Phagein, to eat, Ku- 
tos, cell and osis, condition of.) The 
active functioning of phagocytes. A 
blood cell that ingests and destroys 
harmful matter in the tissues.) 

Phlebolith (Gr.Phlebs, a vein and Li- 
thos, a stone.) A calculus or con- 
cretion in a vein. 

Phlegmonous (Gr.Phlegmone, phleg- 
mon.) Pertaining to phlegmon. (An 
inflammation characterized by the 
spreading of purulent fluid in the 
tissues. 

Phosphorescence (Gr.Phosphoros, phos- 
phorous.) The emission of light 
without appreciable production of 
heat. 

Photogenic (Gr.Photos, light and Gen- 
naein, to produce.) Causing or pro- 
ducing light. 

Physiology (Gr.Phusis, nature and Lo- 
gos, study.) The study of the func- 
tions of the organs of the living 
body. 

Phytoparasite (Gr.Phutos, plant. Para, 
near and Sitos, food.) A parasite 
vegetable organism. 

Pigmented (L.Pingere, to paint.) A con- 
dition to deposition of coloring 
matter in the tissues. 

Placental (Gr.Plakous, a cake.) Per- 
taining to the placenta. The organ 
of the uterine wall to which the 
foetus is attached and from which 
it obtains its nourishment. 

Placentoma (Gr.Plakous, a cake and 
Oma, a tumor.) A tumor composed 
of placental tissue. 

Pleomorphism (Gr Pleon, more and 
Orphe, form.) The state of having 
more than one form. 

Plexiform (L. Plexus, braid and Porma, 
form.) Having the appearance or 
structure similar to a Plexus. (A 
network of vessels.) 

Plumbosis (L.Plumbum, lead and osis, 
a condition of.) A condition of poi- 
soning by or deposition of lead in 
the tissues 



Pneumonokoniosis (Gr.Pneumon, lung 
and Konia, dust, osis a condition 
of.) A condition of chronic indura- 
tion in the lung tissues due to the 

deposition of inhaled dust. 

Post-natal (L.Post, after and Nansisci, 
to be born.) Occuring after birth. 

Polar (Gr.Polos, pole.) Pertaining to a 
pole. (Either extremity of an axis.) 

Palydactylism (Gr.Polus, many and 
Dektulos, finger.) The condition of 
having many digits. 

I olygonal (Gr.Polus, many and Gonos, 
angle.) Having many angles or 
sides. (Spoken of a surface.) 

Polyhedral (Gr.Polus, many and Hedra. 
side.) Having many sides or sur- 
faceiS. (Spoken of a solid.) 

Polymeric (Gr.Polus, many and Meros, 
part.) Pertaining to the existence of 
a large number of parts. 

Polymorphonuclear (Gr.Polus, many, 
Morphe, form and L. Nucleus, nuc- 
leus.) Having nuclei of many forms 

Potential (L.Potens, powerful.) Cap- 
able of doing work or of acting. 

Predisposition (L.Prae, before, Dis, 
apart and Ponere. to place.) The 
condition of liability to acquire a 
disease. 

Primitive (L.Primus, first ) First In 
point of time: Original. 

Progeny (Gr.Pro, before and Gennaein, 
to produce.) Offspring or descend- 
ents. 

Progressive (LPro, before and Gredl, 
to step.) Gradually advancing or 
moving forward. 

Prolapse (L.Pro. forward and Labi, to 
slip.) The falling downward or for- 
ward of a part. 

Proliferate (L.Pro. forward an Ferre, to 
bear.) To form new tissue of the 
same kind (usually excessive.) 

Prolific (L.Pro, forward and Labi, to 
slip.) The quality of being able to 
proliferate. 

Prophase (Gr.Pro, before and' Phasis, 
phase.) The first stage in indirect 
cell division (Mitosis.) 

Proteoses (Gr.Protos, first.) Substances 
formed in gastric digestion and into 
intermediate between a proteid and 
a peptone. 

Protoplasm (Gr.Protos, first and Plasse- 
in, to mold.) The viscid, essential 
substance of a living cell. 

Prototype (Gr.protos, first and Tupos, 
type.) An original type, one after 
which others are copied. 

Protozoa (Gr.Protos, first and Zoon, ani- 
mal.) A class of unicellular, animal 
microorganisms. 

Pseudo (T.,Psoudo. false.) i^'alse. 



GLOSSARY. 



385 



Peorospermic (Gr. Psora, Itch and Hper- 
ma, seed.) Of the nature of or like 
a Psorosperm A protozoon. A 
coccidium. 

Ptomain (Gr.Ptoma, a corpse.) A pro- 
duct formed in the decomposition of 
dead animals tissues. 

Purulent (L.Pus. pus.) Of the nature or 
associated with pus, upon a sur- 
face. 

Pus (L Pus, pus.) Liquefied, necrotic tis- 
sue composed of altered leucocytes, 
tissue shreds and usually micropar- 
asites, suspended in a fluid (liquor 
puris. ) 

Pustule (Lf.Pus, and diminutive term.) 
A vesicle containing pus. 

Pyogenic \Gr.Puon, pus and Gennaein, to 
produce.) Capable of producing pus. 

Pyorrhoea (Gr.Puon, pus and Hroia, a 
flow.) A persistent discharge of pus 
upon a surface. 

Pyrexia (Gr.Pur, fire and Hexis, a ha- 
bit.) An abnormal elevation of a 
temperature. (Fever.) 

Radicular (L, Radix, root and diminu- 
tive term.) Pertaining to or like a 
radicle or root. 

Ranula. (L.Rana, frog and diminutive 
term.) A cystic tumor in the mouth 
(especially on the tongue) due to 
the obstruction of a gland-duct. 

Receptors (L.Recipere, to receive.) The 

"Side-chains" of a body cell (Ehrlich's 
side-chain theory.) 

Regeneration (L.Re, again and Genar- 
are, to beget.) The process by 

which destroyed tissues are re- 
placed. 

Remittent (L.Re, back and Mittere, to 
send.) Characterized by abatemnt or 
subsidence or repetition. 

Resorbed (L.Re, again and Sorbere, to 
absorb.) Taken up again into the 
system. Spoken of a substance that 
has passed out and accumulated in 
the tissues. 

Reticular (L.Reticulum, a little net 
(Rete) ). Resembling a net. Formed 
by a net-work. 

Retrogressive (L. Retro, backward and 
Gradus, step.) Of the nature of re- 
trogression. Agoing backward from 
a pre-existing condition. 

Rhabdomyoma (Gr.Rhabdos, a rod, 
Mus, muscle and Oma. tumor.) A 
form of muscle-tumor (Myoma), 
characterized by the presence of 
striated muscle fibres. 

Rhexis (Gr.Rhexis, rupture.) The rup- 
ture of an organ or vessel. 
Rythm (Gr.Hruthmos, rythm.) The re- 



currence of a motion or sound at 
regular intervals. 

Rupture (L.Rumpere, to break.) A con- 
dition of being broken apart by vio- 
lence. 

Sacculate (L.Saccus, a sac and diminu- 
tive term.) To form small sacs. 

Sanica (Li.Sanies.) A thin, fetid, sero- 
purulent fluid discharge from an ul- 
cer, fistula, etc. 

famous (L. Sanies.) Pertaining to or of 
the nature of Sanies. 

Sapremia (Gr.Sapros, rotten and Haima, 
blood. ) The entrance Into the blood 
of the products of putrefactive mi- 
croorganisms. 

Saprogenic (Gr.Sapros, putrid and Gen- 
naein, to produce. ) Causing or pro- 
ducing putrefaction. 

Saprophytic (Gr.Sapros, rotten and Phu- 
tos, plant.) Pertaining to Sapro- 
phytes: (Vegetable organisms living 
on decaying organic matter.) 

Sarcolemma (Gr.Sarx, flesh and Lemma, 
a sheath.) The delicate sheath en- 
veloping a muscle fibre. 

Sarcoma (Gr.Sarx, flesh and Oma, tu- 
mor.) A tumor made up of embryo- 
nal connective tissue cells. 

Schistosis (Gr. Schistos, a cleft and 
osis, a condition of.) A condition of 
being split or cleft. 

Scirrhous (Gr.Skirrhos, hard.) Of the 
nature of a Scirrhus. (A hard tu- 
mor: A Carcinoma.) 

Sclera (Gr.Skleros, hard.) The firm 
outer coat of the eye-ball continuous 
with the cornea and optic nerve. 

Secretion (L.Secernere, to secrete.) The 
process of separating out a substanec 
from the blood. 

Segmentation-cells (L.Segmentum from 
Secare, to cut.) One of the cells of 
an ovum formed by dividing into 
two equal parts. 

Senile (L.Senex, old.) Pertaining to old 
age. 

Sequel (L.Sequi, to follow.) A follow- 
ing upon or a resultant of. 

Sequestration (L.Sequestrare, to separ- 
ate. ) The formation of a sequestrum. 

Sequestrum (L.Sequestrare, to separate.) 
A piece of dead bone that has be- 
come separated from the sound bone 
during necrosis. 

Siderosis (Gr. Sideros, iron and osis, a 
condition of.) A condition of pig- 
mentation by the deposit, especially 
in the lungs, of particles of iron. 

Siluroid (Gr.Siluros, a species of fish.) 
Pertaining to Siluroidei, an order 
of fishes. 

Simultaneous (L.Simul, at the same 



386 



GLOSSARY. 



time.) Existing or happening at the 
same time. 

Sinusoid (L. Sinus, a cavity and old, of 
the nature of.) Like a sinus: (A 
hollow or cavity or tract.) 

Slough (M.E.Slouh, the skin of a snake.) 
A mass of soft tissue destroyed hy 
necrosis. 

Slougrhing: (M.E.Slouh, skin of a 
snake.) The process of becoming a 
slough. 

Soliped (L. Solus, alone and Pes, foot.) 
An animal with a single hoof or 
digit. 

Somatic (Gr.Soma, body) Pertaining to 
the body, especially to the frame- 
work as distinguished from the vis- 
cera. 

Specific (L. Species, species.) Of or per- 
taining to a species. Produced by a 
particular kind of organism. 

Specificity (L. Species, species and Face- 
re, to make.) The quality of being 
specific. 

Spermatogenesis (Gr.Sperma, semen and 
Gennaein, to produce.) The develop- 
ment of Spermatozooa. 

Sphacelus (Gr.sphakelos, dead.) A mass 
of soft tissue destroyed by necro- 
sis. 

Spirem (L.Spira, a coil.) The close or 
mother-skein of chromatin fibrils in 
indirect cell division. (Mitosis.) 

Spongrioplasm (Gr.Spoggos, a sponge and 
Plassein, to mold.) The fine proto- 
plasmic threads forming the reti- 
culum of a cell. 

Spontaneous (L.Spons, will.) Occuring 
without external influence. 

Spore (Gr.Sporos, seed.) A reproductive, 
resting element of lower organisms. 

Sporulation (Gr.Sporos, seed and L.Fer- 
re, to m&.ke.) The production of 
spores. 

Stalactite (Gr.Stalazein, to drop.) A 
pendant cone of calcium salts like 
an icicle. 

Stasis (L. Stare to stand.) A standing 
still or stoppage of motion, espe- 
cially of blood, in a part. 

Stenosis (Gr.Stenos, narrow.) A narrow- 
ing of the lumen of a vessel. 

Sterile (L.Sterilis, barren.) Incapable of 
reproducing. 

Sthenic (Gr.Sthenos, strength.) Char- 
acterized by strength or severity. 

Strata (L. Stratum, stratiyn.) A series 
of layers. 

Stroma (Gr. Stroma, a bed.) The tissue 
forming the ground substance or 
framework for the essential part of 
an organ. Interstitial tissue. 

Suggillation (L.Suggillare, to beat black 



and blue.) An extensive, capillary, 
tissue-hemorrhage. 

Suppuration (L.Sub, under and Pus, 
pus.) The formation of pus. (Sur- 
face or subsurface.) 

Susceptible (L.Sub, under and Cipere, 
to take.) Having a liability to ac- 
quire a disease. 

Swelling: (A.S.Swellan, to grow larger.) 
An elevation or elevated area (spe- 
cially abnormal.) 

Symptom (Gr.Sun, together and Ptoma, 
a falling.) Sequential functional 
disturbances due to disease. 

Syncytium (Gr.Sun, together and Kutos, 
cell.) A fusion of several cells into 
a single cell. 

Syncope (Gr.Sun, together and Kop- 
tein, to strike.) A partial or com- 
plete, temporary suspension of heart 
action. 

Synthesis (Gr.Sun, together and Tithe- 
nai, to put.) The formation of a 
compound by putting together its 
constituents. 

Systole (Gr.Sun, together and Stellein, 
to place.) The period of the heart's 
contraction especially of the ven- 
tricles. — Opposed to Diastole. 

Telophase (Gr.Telos, end and Phasis, 
phase.) The fourth and last stage 
in indirect cell division. (Mitosis.) 

Telangrlectatic (Gr.Telos, end Aggeion, a 
vessel and Ektasis, a dilatation.) Of 
or pertaining to Telangiectasis. (A 
permanent dilatation of groups of 
capillaries aid arterioles. 

Tenable (L.Tenere, to hold.) Able to be 
held or supported. 

Teratoma (Gr.Teras, monster and Oma, 
tumor.) A tumor composed of tis- 
sues derived from all three germ- 
layers. 

Tetanic (Gr.Tetanos, tetanus) Pertain- 
ing to or resembling tetanus. Char- 
acterized by tonic muscular spasms. 

Thermic (Gr.Therme, heat.) Of or per- 
taining to heat. 

Thermogenic (Gr. Thermos, heat and 
Gennaein, to produce.) Pertaining to 
causing or producing heat. 

Thermogenesis (Gi*.Therme, heat and 
Gennaein, to produce. ) The genera- 
tion or production of heat. 

Thermolysis (Gr.Therme, heat and Lue- 
in, to loose.) The loss of heat. 

Thoracischiopa§:u8 (Gr. Thorax, thorax, 
Ischion, hip and Pagos, union.) A 
monster with two heads but with 
bodies and hips united. 

Thrombosis (Gr.Thrombos, a clot and 
osis, a condition of.) A condition of 
the existence of a thrombus. 



GLOSSARY. 



387 



Thrombus (Gr.Tlirombos, a clot.) A coa- 
gulum formed within a living blood- 
vessel. 
Tolerance (L. Tolerate, to endure.) Abil- 
ity to endure the continuation of an 
act. 
Tonic (Gr.Tonikos, tone.) Pertaining to 
tone. Characterized by continuous 
tension or contraction, or an agent 
that tends to restore normal tone. 
Tophi (Gr.Tophos, a stone.) Hard stone- 
like deposits. 
Torsion (L.Torquere, to twist.) A twist- 
ing or the act of twisting. 
Toxin (Gr.Toxikon, a poison.) A nitro- 
genous product formed by cells. 
Bacterial toxin. 
Transudate (L.Trans, through and Su- 
dare, to sweat.) A fluid that has 
passed through a membrane. Espe- 
cially non-inflammatory blood serum 
that has passed through vessel 
walls. 
Transudation (L.Trans, through and 
Sudare, to sweat.) The production 
of a transudate. 
Traumatism (Gr. Trauma, a wound and 
ism, a condition of.) A condition 
due to an injury or wound. 
Tricephalus (Gr.Tris, three and Kep- 
hale, head.) A monster having three 
heads. 
Trophic (Gr. Trophic, food.) Pertaining 

to nutrition. 
Tubercle (L.Tuber, a swelling and dim- 
inutive term.) A small nodule. 
Tnmefled (L.Tumere, to swell and Fa- 
cere, to make.) In a swollen condi- 
tion. 
Tumor (L. Tumere, to swell.) A morbid 
enlargement. A growth of new tis- 
sue non-inflammatory, .persistent and 
independent of the surrounding 
structures, atypical in structure and 
function. 
tlcer (L. Ulcus.) A denuded surface re- 
sulting from a continuous and some- 
times progressive cellular necrosis. 



Ulceration (L. Ulcus, an ulcer.) The for- 
mation of an ulcer. 
Ultramicroscopic (L. Ultra, beyond, Gr.- 
Mikros, small and Skopeein, to look 
at.) Too small to be seen with a 
microscope. 
Uniparous (L.Unus. one and Parere, to 
produce.) Bringing forth one off- 
spring at a birth. 
Vaccine (L.Vacca, cow.) An attenuated 
virus used for inoculation purposes. 
Vacuolated (L. Vacuus, empty.) A condi 

tion of the presence of vacuoles. 
Vacuole (L. Vacuus, empty.) A space or 
cavity in the protoplasm of a cell. 
Vascularization (L.Vasculum, a small 
vessel.) The process of becoming 
vascular or of being supplied with 
vessels. 
Vehicle (L.Vehere, to carry.) A sub- 
stance serving to carry or hold an- 
other. 
Vesicle (L. Vesica, a bladder and dimin- 
utive term.) A circumscribed accu- 
mulation of inflammatory serous 
exudate in the deeper layers of the 
epidermis or of the mucosa, usually 
about pinhead size. 
Villus (L. Villus, a tuft of hair.) One of 
the minute projections of the mu- 
cous membrane of the intestinal 
.canal. 
Virulency (L. Virus, a poison.) Pertain- 
ing to extreme poisonousness, dis- 
ease producing power or strength. 
Virulent (L. Virus, a poison.) Very pow- 
erful or Poisonous. 
Vitiligo (L. Vitiligo, vitiligo.) A skin- 
disease characterized by disappear- 
ance of normal pigment in patches. 
Volvulus (L.Volvere, to roll.) A Twist- 
ing of an organ so as to occlude its 
lumen. 
Wound (A.g.Wund, wound.) The result 
of the sudden interruption of the 
Continuity of a tissue or tissues. 
Zymogenic (Zume, leaven and Genna- 
ein, to produce.) Causing or per- 
taining to fermentation. 



INDEX 



Abdomino-schisis, g8. 

Abscess, cold, 170. 

Abscess formation, 169. 

Abscess, hot, 170. 

Abscess, metastatic, 170. 

Absorption of necrotic tissue, 261. 

Acardia, 93. 

Acaudia, 94. 

Acephalus, 93. 

Achorion Schoenleini, 49. 

Achromatosis, 249. 

Acidophiles in inflammation, 152. 

Acme, fever, 341. 

Acquired disease, 2)7' 

Acquired immunity, 82. 

Acquired immunity theories, 87. 

Acromegaly, 190. 

Actinomycosis, 355. 

Avenue of entrance, 357. 

Differential diagnosis, 360. 

Distribution, 355. 

Etiology, 356. 

Extension, 360. 

Lesions, 358. 

Source of infection, 356. 

Susceptible animals, 355. 
Active and acquired immunity, 83. 
Acute disease, 35. 
Acute inflammation, 173. 
Adenoma, 326. 
Adenoma clinically, 327. 
Adenoma, microscopic, 326. 
Adeno-sarcoma, 328. 
Adeno-sarcoma, microscopic, 329. 
Adipose absorption, 204. 
Adipose depositories, 203. 
Adipose digestion, 204. 
Adipose regeneration, i8t. 



Aerobic bacteria, 58. 

Agastria, 93. 

Agglutination test, glanders, 368. 

Agnathus, 94. 

Albino, 249. 

Alveolar-sarcoma, 309. 

Amboceptor, 90, 91. 

Amelus, 94. 

Amitosis, 24. 

Amputation neuroma, 182. 

Amylus, 93. 

Amylin, 210. 

Amyloid formation, 211. 

Amyloid formation appearance, 211. 

Amyloid formation, cause, 211. 

Amyloid formation, effects, 211. 

Amyloid formation, tissue affected, 

2\\. 

Amyloid reaction, 210. 

Amyloid test, 211. 

Anabolism, 31. 

Anserobism, 58. 

Anaphase, 28. 

Anasarca, 120. 

Anatomical alterations, heart, iio. 

Anemia, 132. 

Angioma, 293. 

Anhydremia, 112. 

Anomalies, 92, 

Ante-natal disease, yj- 

Ante-natal hypertrophy, 189. 

Anthracosis, 248. 

Aplasia, 93. 

Apnoea, ']j. 

Apoplexy, 'jj. 

Aprosopus, 94. 

Apus, 94. 

Argyriasis, 248. 

Arrested development, 93. 



388 



INDEX. 



389 



Arteriolith, 238. 

A.rterioclerosis, iii. 

Arthropoda, 69. 

Ascites, 119. 

Aspergillus fumigatus, 50. 

Aspergillus, niger, 51. 

Asthenic fever, 342. 

Atheroma, S27- 

Atheromatous degeneration, 229. 

Atresia, 99. 

Atresia anus, 99. 

Atresia iridis, 99. 

Atresia oculi, 09. 

Atresia oris, 99. 

Atresia urethra, 99. 

Atrichia, 93. 

Atrophy, 196. 

Atrophy, appearance, 198. 

Atrophy, cause, 197. 

Atrophy, effects, 199. 

Atrophy, pathologic, 197. 

Atrophy, physiologic, 197. 

Atrophy, senile, 197. 

Autosite, 109. 

Avian tubercular lesion, 352. 

Axone, rate of grov^th, 182. 

Axone regeneration, 182. 



Bacilli, 53. 

Bacteria, 52. 

Bacterial immunity, 86. 

Bacterial pigmentation, 60. 

Bacterial proteids, 62. 

Bacterial toxins, 61. 

Bacterium mallei, 362. 

Bacterium tuberculosis, 345. 

Bacterium necrophorus, 253, 254. 

Basophiles, 152. 

Benign tumors, 275. 

Bile concrement, 240. 

Biliar calculi, 236. 

Birth mark, 294. 

Blister, 42. 

Blister test, 265. 

Blood flow in inflammation, 147. 

Blood oscillation, 148. 



Blood pressure, ill. 

Blood quality, iii. 

Blood, quantity, III. 

Blood regeneration, 178. 

Blood stasis. 149. 

Blood vessel regeneration, 178. 

Bovine tubercular lesions, 360. 

Bursattae, 251. 



Calcareous infiltration, 227. 

Calcareous infiltration, appearance, 
228. 

Calcareous infijtration, cause, 22^. 

Calcareous infiltration, effects, 229. 

Calcareous infiltration, tissue affect- 
ed, 229. 

Calculi, 230. 

Calculi arteries, 238. 

Calculi bile ducts, 236. 

Calculi, cause, 230. 

Calculi, color, 231. 

Calculi, composition, 231. 

Calculi, fcEtus-litho pedium, 238. 

Calculi, gall bladder, 2^6. 

Calculi, intestine, 236. 

Calculi, kidney, pelvis, 233. 

Calculi, mammary ducts and sinuses, 

237_- 
Calculi, number, 231. 
Calculi of prepuce, 235. 
Calculi of salivary gland ducts, 235. 
Calculi, shape, 231. 
Calculi, size, 231. 
Calculi, structure, 231. 
Calculi, stomach, 236. 
Calculi, ureter, 234. 
Calculi, urethra, 234. 
Calculi, urinary bladder, 234. 
Calculi, uriniferous tubules, 233. 
Canalization, 178. 
Cancellated osteoma, 288. 
Carcinoma, 320. 
Carcinoma, clinically, 323. 
Carcinoma, differentiation, 323. 
Carcinoma, encephaloid, 320. 
Carcinoma, metastasis, 323. 



390 



INDEX. 



Carcinoma, microscopic, 322. 

Carcinoma, scirrhus, 321. 

Capillary telangiectasis, 294. 

Cartilage regeneration, 180. 

Cartilage tumor, 283. 

Caseation necrosis, 257. 

Castration, fatty changes, 205. 

Catarrhal inflammation, 174. 

Cavernous hemangioma, 294, 

Cell, definition^ 20. 

Cell growth, 23. 

Cell motion, 29. 

Cell reproduction, 24. 

Cell shape, 23. 

Cell size, 2$. ' ■> 

Cell structure, 21. 

Cell waste, 32. 

Cementoma, 294. 

Centrosome, 22. 

Cerumenous concrements, 24T. 

Cervical ectopia cordis, 103. 

Cheiloschisis, 96. 

Chemical causes of disease^ 44. 

Chemical composition of exudate, 150. 

Chemical necrosis, 253. 

Chemical reaction, cloudy swelling, 

200. 
Chemical reaction, retrograde 

changes, 195. 
Chemotaxis, 159. 
Chilblains, 144. 
Cholelith, 236. 
Cholesteatoma, 335. 
Chondroma, 283. 
Chondroma, clinically, 285. 
Chondroma, microscopic, 284. 
Chondro-sarcoma, 317. 
Chorio-carcinoma, 331. 
Chorio-epithelioma, 331. , 
Chromosome,'! 27. ,, ,, 

Chronic disease, 35. 
Chronic inflammation, 173. 
Chylous ascites, 117. 
Cicatrization, 185. 
Cilia, -31. 

Circulatory disturbances, no. 
Cirsoid hemangioma, 295. 



Cladothrix actinomyces, 356. 
Cloacal persistence, 103. 
Cloudy swelling, 200. 
Clody swelling, appearance, 202. 
Cloudy swelling, cause, 200. 
Cloudy swelling, effects, 202. 
Cloudy swelling, tissue affected, 202. 
Coagulation necrosis, 256. 
Cobra, 48. 
Coccidium, ^71. 
Coccus, 53. 

Colliquation necrosis, 256. 
Colloid formation, 217. 
Colloid formation, appearance, 218. 
Colloid formation, cause, 217. 
Colloid formation, effects 220. 
Colloid tests, 217. 
Color blending, 35. 
Compensatory hypertrophy, 188. 
Complement, 90, 91. 
Complete duplicates, 106. 
Composite odontoma, 293. 
Compound follicular odontoma, 292. 
Concentric hypertrophy, 188, 
Concrements, 238. 
Concrements, bile, 240. 
Concrements, cerumen, 240. 
Concrements, fecal matter, 239. 
Concrements, hair, 238. 
Concrements, milk, 240. 
Concrements, parasitic, 241. 
Concrements, pus, 240, 
Concrements, source, 238. 
Congenital diseases, 37. 
Connective tissue regeneration, 179. 
Contiguity, 75. 
Continued fever, 342. 
Continuity, 75. 
Convalescence, fever, 341. - 
Corneal, reaction, 141. 
Cornification, 224. 
Corrosive poisoning, 44. 
Craniopagi, 107. 
Craniorrachischisis, 95. 
Cranioschisis, 95. . . 

Crisis, 341. , 

Cyclopia, 98. 



INDEX. 



391 



Cysts, 335. 

Cysts, degeneration, 2>Z7- 
Cysts, dermoid, 338. 
Cysts, extravasation, 2>Zy. 
Cysts, exudation, 2>2>7- 
Cysts, multilocular, 335. 
Cysts, parasitic, 2>2>7- 
Cystic calculi, 234. 
Cystoma, 335. 



Death, yj, 262. 

Death, pathologic, 263. 

Death, physiologic, 262. 

Death signs, 264. 

Death tests, 265. 

Decomposition, 265. 

Deciduoma malignum, 331. 

Decline, fever, 2>2,7- 

Degeneration cysts, 334. 

Dentigerous cysts, 334. 

Dentine regeneration, 181. 

Depigmentation, 250. 

Dermoid cysts, 333. 

Diabrosis, 113. 

Diapedesis, 113. 

Dicaudis, 100. _ 

Dicephalus, 108. 

Diphtheritic inflammation, 171. 

Diplo-coccus, 53. 

Dipygusamelus, 94. 

Dislocation, 40. 

Direct cell division, 24. 

Disease, 35. 

Disease extension, 74. 

Disease termination, 75. 

Dropsy, 118. 

Duplicities, assymetrical, 107. 

Duplicities, free, 106. 

Duplicities, incomplete, 107. 

Duplicities, monochorionic, 106. 



Eburnated osteoma. 
Ectopia gastrium, 98 
Egagaropile, 238. 



Ehrlich's lateral chain theory, 87. 

Electric causes of disease, 44. 

Embolism, 128. 

Embolism, effects, 130. 

Embolus, 128. 

Embolus air, 128. 

Embolus, bacterial, 128. 

Embolus cells, 128. 

Embolus, location, 129. 

Embolus, parasitic, 128. 

Embolus, thrombic fragments, 128. 

Embryonic epithelial tumors, 321. 

Empyemia, 170. 

Encapsulation of necrotic tissue, 261. 

Encephaloid carcinoma, 321. 

Endermic goitre, 218. 

Endothelial cells in inflammation, 

152. 
Endothelioma, 310. 
Endotoxins, 62. 
Enterolith, 236. 
Enterorrhagia, 115. 
Ephemeral fever, 342. 
Epistaxis, 114. 
Epithelial odontoma, 291. 
Epithelial pearls, 225. 
Epithelial regeneration, 181, 182. 
Epithelioma, 324. 
Epithelioma, clinically, 326. 
Epithelioma, microscopic, 325. 
Epithelioma, pearl, 325. 
Epithelioma, seritonale, 331. 
Epithelioma contagiosum, 370. 
Epithelioma contagiosum, cause, 371. 
Epithelioma contagiosum, lesion, 

371, 372. 
Epithelization, 185. 
Ergot, 46, 255. 

Erythrocytes in inflammation, 152. 
Etiology, 19. 
Etiology of disease, 38. 
Exciting cause of disease, 40. 
Exfoliation, 261. 

Exhaustion theory of immunity, 87. 
Exophthalmic goitre, 217. 
Extension of disease, 74. 
Extravasate, 184. 



392 



INDEX. 



Extravasation cysts, ^37. 
Exuberant granulation, 187. 
Exudate, 150. 
Exudate, cause, determining kind, 

155- 
Exudate, chemical composition, 150. 
Exudate, histological composition, 

151- 

Exudate, effects, 155, 157. 

Exudate, fibrinous, 154. 
Exudate, hemorrhagic, 154. 
Exudate, purulent, 155. 
Exudate, serous, 154. 
Exudate, significance of, 156. 
Exudation cyst, 337. 



Fibrinous exudate, 154. 
Fibroblasts, 179. 
Fibroma, 278. 
Fibroma, clinically, 280. 
Fibroma, differentiation, 281. 
Fibroma, hard, 279, 
Fibroma, soft, 280. 
Fibro-sarcoma, 312. 
Fibrous hyperplasia, 192. 
Fission, 56. 
Fistulous tracts, 170. 
Flagella, 54. 

Follicular odontoma, 291, 
Focal necrosis, 259. 
Fracture, 40, 183. 
Fracture, repair, 180. 
Freckles, 247. 
Function, variations, 196, 197. 



Fatty changes, 203. 

Fatty changes, pathologic, 207. 

Fatty changes, pathologic, appear- 
ance, 208. 

Fatty changes, pathologic, cause, 207. 

Fatty changes, pathologic, effects, 210. 

Fatty changes, Physiologic, 205. 

Fatty changes, physiologic, appear- 
ance, 206. 

Fatty changes, physiologic, cause, 205. 

Fatty changes, physiologic, effects, 
206. 

Fatty infiltration, 205. 

Fatty necrosis, 258. 

Favus, 49. 

Fecal concrements, 239. 

Fever, 339. 

Fever, acme, 341. 

Fever, asthenic, 342, 

Fever, continuous, 342, 

Fever, convalescence, 341. 

Fever, course, 340. 

Fever, decline, 341. 

Fever, ephemeral, 341. 

Fever, intermittent, 342. 

Fever, onset, 340. 

Fever, sthenic, 342. 



Gangrene, 257. 

Gastric calculi, 236, 

Gastroliths, 236. 

General diseases, 38. 

Giantism, 189. 

Glanders, 361. 

Glanders, agglutination test, 368. 

Glanders, avenue of infection, 362. 

Glanders, cause, 362. 

Glanders, diagnosis, 368, 369. 

Glanders, lesions, 363. 

Glanders, mallein test, 368. 

Glanders, course of infection, 362. 

Glioma, 289. 

Glycogen, 221. 

Glycogen composition, 221. 

Glycogen tests, 221. 

Glycogenic infiltration, 221. 

Glycogenic infiltration, appearance, 

222. 
Glycogenic infiltration, cause, 222. 
Glycogenic infiltration, effects, 222. 
Goitre, 217. 
Granulation, 185. 
Granulation, exuberant, 187. 
Growth of tumors, 272, 



INDEX. 



393 



H 

Hair balls, 238. 

Haptophores, 89, 90, 91. 

Health, 35. 

Healing by primary union, 184. 

Healing by granulation, 185. 

Heart anatomical changes, no. 

Heart diminished action, no. 

Heart increased action, no. 

Helminthes, 63. 

Helminthes response to stimuh, 140. 

Hemangioma, 294. 

Hemangioma cavernosum, 294. 

Hemangioma cirsoid, 295. 

Hemangioma hyperthophicum, 295. 

Hemangioma simplex, 294. 

Hemangiosarcoma, 318. 

Hematemesis, 114. 

Hematidrosis, 115. 

Hematocele, 115. 

Hematogenous pigmentation, 243. 

Hematoma, 115. 

Hematometra, 115. 

Hematuria, 115, 

Hemic poisons, 45. 

Hemocoelia, 114. 

Hemoglobin in pigmentation, 244. 

Hemolysis, 343. 

Hemophilia, 112. 

Hemopt3-sis, 114. 

Hemorrhage, yy, 112. 

Hemorrhage, cause, 113. 

Hemorrhage, ecchymotic, 114. 

Hemorrhage, epistaxis, T14, 

Hemorrhage, effects, 115. 

Hemorrhage, petechial, 113. 

Hemorrhage, suggillation, 114. 

Hemorrhagic exudate, 154. 

Hemosiderin, 245. 

Hemotoidin, 245. 

Hemothorax, 115. 

Hepatogenous pigmentation, 246. 

Heredity, 35. 

Heredity in fatty changes, 205. 

Hermaphroditism, 103. 

Hermaphrodite, bilateral, 104. 

Hermaphrodite, lateral, 104. 



Hermaphrodite, false, 104. 

Hermaphrodite, true, 104. 

Hermaphrodite, unilateral, 104. 

Hernia, 40. 

Histoid tumor, 269. 

Humoral theory of immunity, 89. 

Hyalin, 212. 

Hyalin, chemical composition, 213. 

Hyaline formation, 212. 

Hyaline formation, appearance, 213. 

Hyaline formation, cause, 213. 

Hyaline formation, effects, 214. 

Hydrargirosis, 248. 

Hydrops, 118. 

Hydrothorax, 119. 

Hydropericardium, 119. 

Hydrocele, 119. 

Hydrocephalus, 119. 

Hyperchromatosis, 243. 

Hyperaemia, 113. 

Hypersemia, arterial, 135. 

Hypersemia, arterial, appearance, 136. 

Hypersemia, arterial, cause, 135. 

Hypersemia, arterial, effects, 136. 

Hypersemia, arterial, pathologic, 137. 

Hyperaemia, arterial, physiologic, 137. 

Hypersemia, arterial, therapeutic, 

137- 
Hypersemia, Bier's, 134. 
Hypersemia, venous, 133. 
Hyperaemia, venous, appearance, 133. 
Hyperaemia, venous, cause, 133. 
Hypersemia, venous, effects, 134. 
Hypersemia, venous, pathologic, 134. 
Hypersemia, venous, therapeutic, 134. 
Hypernephroma, 329. 
Hyperplasia, 188. 
Hyperplasia, appearance, 192. 
Hyperplasia, cause, 192. 
Hyperplasia, effects, 193. 
Hyperplasia, fibrous, 192. 
Hyperplasia, interstitial, 191, 192. 
Hyperplasia, parenchymatous, 191. 
Hypertrophy, 188. 
Hypertrophy, ante natal, 189. 
Hypertrophy, appearance, 190. 
Hypertrophy, cause, i8q. 



394 



INI>EX. 



Hypertrophy, compensatory, i88. 
Hypertrophy, concentric, i88. 
Hypertrophy, effects, 190. 
Hypertrophy, general, 189. 
Hypertrophy, inherited, 189. 
Hypertrophy, numerical, 192. 
Hypertrophy, post natal, 189. 
Hypertrophy, false, 188. 
Hypochromatosis, 249. 
Hypoplasia, 93, 94. 



Icterus, 246. 

Immediate union, 184. 

Immunity, 78. 

Immunity, acquired, 82. 

Immunity, active acquired, 83. 

Immunity, bacterial, 86. 

Immunity, inherited, 80. 

Immunity, passive, 86. 

Immunity, toxic, 84. 

Inanition, necrosis, 254. 

Incision test, 265. 

Indirect cell division, 26. 

Infarct, 131. 

Infarct, anemic, 131. 

Infarct, hemorrhagic, 131. 

Infarction, 131. 

Infective granulomata, 341. 

Inflammation, 138. 

Inflammation, acute, 173. 

Inflammation, catarrhal, 174. 

Inflammation, causes, 143. 

Inflammation, chronic, 173. 

Inflammation, croupous, 171. 

Inflammation, diphtheritic, 171. 

Inflammation, effects, 161, 

Inflammation, factors concerned in, 

146. 
Inflammation, hemorrhagic, 172. 
Inflammation, infective, 167. 
Inflammation, interstitial, 173. 
Inflammation, non-suppurative, 167. 
Inflammation, parenchymatous, 173. 
Inflammation, phlegmonous, 170. 



Inflammation, proliferative, 174. 
Inflammation, purulent, 169, 174. 
Inflammation, pustular, 174. 
Inflammation, signs, 160. 
Inflammation, simple, 166. 
Inflammation, specific, 174. 
Inflammation, suppurative, 167. 
Inflammation, termination, 174, 175, 
Inflammation, ulcerative, 174. 
Inflammation, vascular changes, 146, 

147, 148. 
Inflammation, vesicular, 174. 
Inflammatory exudate, 150. 
Inflammatory exudation, 149. 
Inherited disease, 35. 
Inherited epilepsy, 2)7- 
Inherited immunity, 80. 
Inherited malformations, 36. 
Inherited ophthalmia, 2)1' 
Inherited tumors, 2,^. 
Inspissated bile, 240. 
Inspissated pus, 240. 
Intermittent fever, 342. 
Interstitial hyperplasia, 191, 192 
Interstitial inflammation, 170. 
Interstitial expansion, tumor, 272. 
Intestinal calculi, 236. 
Involucre, 261. 
lodothyreoglobulin, 217. 
Irritability, 32. 
Irritant, 139. 
Ischiopagus, 107. 
Ischiopagus parasiticus, 107. 



Jack sores, 260. 



Karyokinesis, 26. 

Katabolism, 31. 

Keloid, 281. 

Keratosis, 224. 

Keratosis, appearance, 225. 

Keratosis, cause, 224. 

Keratosis, effects, 225. 



INDEX. 



395 



Lactation a factor in fatty changes, 

205. 
Lacteal calculi, 237. 
Lacteal concrements, 241. 
Lamellae formation, 181. 
Larkspur, 46. 
Leiomyoma, 296, 297. 
Lesion, 19. 

Leucocytes in inflammation, 151. 
Leucocytes, basophillic, 152. 
Leucoc3'tes, eosinophyllic, 151. 
Leucocytes, neutrophyllic. 151. 
Leucocytic margination, 150. 
Leucoderma, 250. 
Leucomains, 48. 
Lipoma, 285. 
Lipoma, clinically, 287. 
Lipoma, microscopically, 287. 
Liquor puris, 155. 
Lithopedia, 238. 
Local disease, 38. 
Loco, 47. 
Luxation, 40. 

Lymphocytes in inflammation, 153. 
Lymphangioma, 296. 
Lymphorrhagia, 117. 
Lymphorrhagia, cause^ 117. 
Lymphorrhagia, effects, 117. 
Lymphomata, 303, 
Lymphosarcoma, 303. 
Lysis, 341. 

M 

Malformations, 92. 
Malformations, atypical, 93. 
^Malformations, multiple, loi. 
^Malformations, single, 93. 
Malformations, typical, 93. 
Malign tumor, 275. 
Mallein, 368. 
^lalleination, 368. 
Margination, leucocytic, 150, 
Mechanic causes of disease?, 40. 
^lelanin, 247. 
Melano-sarcoma, 315. 



Melanosis, 247. 

IMembrane, cell, 22. 

^Meningocele, 96. 

^letabolism, 31. 

^Metaphase, 27. 

Metaplasia, 193. 

iMetastases, carcinoma, 323. 

IMetastatic tumor, 272. 

Metrorrhagia, 115. 

Microcardia, 94. 

Microcephalus, 94. 

Micrococcus, 53. 

Micrognath}^, 94. 

Micromelus, 95. 

jMicroophthalmia, 94. 

Miliar tubercle, 349. 

Mirror test, 265. 

Mitosis, 26. 

IMixed cell sarcoma, 308. 

Mole, 93. 

IMonophygus amelus, 94. 

Monophygosapus, 94. 

Monothorracisamelus, 94. 

Monothoracisapus, 94. 

Moribund stage fever, 341. 

Mosaic coloring, 35. 

IMoulds, 49. 

Movement, amoeboid, 30. 

Movement, ciliar, 31. 

Movement, intracellular, 29. 

Mucoid changes, 214. 

Mucoid changes, appearance, 215. 

Mucoid changes, causes, 215. 

Mucoid changes, effects, 216. 

IMucoid changes, pathologic, 215. 

Mucoid changes, physiologic, 214. 

Mucoid tissue regeneration, 179. 

Mucus, 214. 

Multilocular cysts, 335. 

IMultiplicit}-, loi. 

IMummifying necrosis, 257. 

Muscular tissue regeneration. 182. 

Myeloid sarcoma, 306. 

Myelomeningocele, 96. 

Myocarditis, no. 

M\-oma, 296. 

Myositis ossificans, 226. 



o:>'o 



INDEX. 



Myxoedema, 215. 
Myxoma, 282. 
Myxoma clinically, 283. 
Myxoma miscropically, 282. 
Myxosarcoma, 316. 

N 

Necrobiosos, 251. 
Necrosis, 251. 
Necrosis caseation, 257. 
Necrosis chemical, 253. 
Necrosis, coagulation, 256. 
Necrosis colliquation, 256, 
Necrosis fatty, 258. 
Necrosis ^ocal, 259. 
Necrosis inaniation, 254. 
Necrosis mumm.ifying, 257. 
Necrosis putrefying, 257. 
Necrosis senile, 258. 
Necrosis subsurface, 256. 
Necrosis surface, 256. 
Necrosis thermic, 254. 
Necrotic stomatitis, 251. 
Nerve tissue regeneration, 182. 
Neuroma, 293. 
Neuromata amputation, 182. 
Neurotoxic poison, 45. 
Neus, 294. 
Neutrophile, 15,1. 
Nucleus, 22. 

Numerical hypertrophy, 191. 
Nutritive disturbances in atrophy, 
197. 



Obstructive necrosis, 252. 
Ochronosis, 245. 
Odontoma, 289. 
Odontoma composite, 293. 
Odontoma compound follicular, 292. 
Odontoma, epithelialj 291. 
Odontoma fibrous, 291. 
Odontoma follicular, 291. 
Odontoma, radicular, 293. 
Oedema, 148. 
Oedema appearance, 120. 
Oedema cause, 118. 



Oedema effects, 121. 

Oedema varieties, 119. 

Olein, 203. 

Onset fever, 340, 

Ospora porrigenes, 48. 

Ophthalmic tubercular test, 355. 

Organoid tumor, 269. 

Osseous regeneration, 180. 

Ossification, 226. 

Ossification appearance, 226. 

Ossification cause, 226. 

Ossification effects, 226. 

Osteoblasts, 180. 

Osteoclasts, 180. 

Osteoma, 288. 

Osteoma cancellated, 288. 

Osteoma clinically, 289. 

Osteoma eburnated, 288. 

Osteoma microscopic, 289. 

Osteo-cystoma dentiferuiji capsular, 

292. 
Osteophytes, 226. 
Osteo sarcoma, 318. 



Palatoschisis, 96. 
Palmatin, 203. 
Papilloma, 318. 

Parasitic causes of disease, 48. 
Parasitic cysts, 22>7- 
Parasitic theory of tumors, 2y6. 
Parenchymatous degeneration, 220. 
Parenchymatous hyperplasia, 191. 
Parenchj^matous inflammation, 173. 
Parenchymatous poisons, 44. 
Partial recovery, yy. 
Pathogenesis, 19. 
Pathology definition, 19. 
Pathology comparative, 19. 
Pathology general, 19. 
Pathology human, 19. 
Pathology special, 19. 
Pathology veterinary, 19. 
Pathologic anatomy, 19. 
Pathologic atrophy, 197. 
Pathologic death, 263. 
Pathologic physiology, 19. 



INDEX. 



397 



Pearl cell epithelioma, 325. 

Peripheral infiltration, 272. 

Persistent foetal structures, 103. 

Phagocyte, 159. 

Phagocytosis, 159. 

Phagocytosis theory, 87. 

Phlebolith, 237. 

Phlegmonous inflammation, 170. 

Phosphorescence, 60. 

Photic cause of disease, 43. 

Ph3^sic cause of disease, 42. 

Phyto-parasites, 48. 

Phj'to-toxin, 79. 

Pigmentary changes, 241. 

Pigmentation bile, 246, 

Pigmentation carbon, 248. 

Pigmentation cells, 247. 

Pigmentation effects, 249. 

Pigmentation hemoglobin, 243. 

Pigmentation hemosiderin, 245. 

Pigmentation, hemotoidin, 245. 

Pigmentation Iron, 248. 

Pigmentation lead, 248. 

Pigmentation mercury, 248. 

Pigmentation, silver, 248. 

Placentoma, 331. 

Plumbosis, 248. 

Pneumomycosis aspergillosis, 50. 

Pneumonokoniosis, 248. 

Porcine tubercular lesion, 351. 

Polydactylism, 100. 

Polumelusthoracicus, 100. 

Poison, 44. 

Post mortem staining, 264. 

Post natal disease, 38. 

Post natal hypertrophy. 189. 

Predisposition, 35. 

Predisposing causes of disease, 38-40. 

Predisposing causes of age, ;^S. 

Predisposing causes of breed, 39. 

Predisposing causes of climate, 39. 

Predisposing causes of color, 39. 

Predisposing causes of food and 

water, 40. 
Predisposing causes of genus, 39. 
Predisposing causes of imitation, 40. 
Predisposing causes of location, 39. 



Predisposing causes of occupation, 
40. 

Predisposing causes of overwork, 40. 

Predisposing causes of previous dis- 
ease, 40. 

Predisposing causes of season, 39. 

Predisposing causes of sex, 39. 

Preputial calculi, 235. 

Pressure atrophy, 196. 

Primary tumors, 272. 

Progressive tissue changes, 177. 

Proliferative inflammation, 174. 

Prophase, 26. 

Prostatic concrements, 241. 

Protoplasm, 20- 

Provisional callous, 181. 

Protozoa, 63. 

Protozoa response to stimuli, 140. 

Psuedo-hermaphrodite, 104. 

Pseudo-hypertrophy, 188. 

Ptomains, 6t. 

Purulent inflammation, 169-174. 

Putrefaction, 61. 

Pus, 155-167-168. 

Pus concrements, 240. 

Pustule, 170- 

Pustular inflammation, 174. 

P3^gopagus, 106. 

Pyorrhoea, 169. 

Pyrexia, 339. 



Rachischisis, 95. 

Ranulae, }27- 

Rattlesnake, 48. 

Reaction aseptic injury, 142. 

Reaction, septic injury, 142. 

Receptor, 89-90-91. 

Recovery, 75. 

Regeneration, 177. 

Regeneration adipose, 181. 

Regeneration blood, 178. 

Regeneration blood vessels, 178. 

Regeneratinn cartilage, 180. 

Regeneration connective tissue, 179. 

Regeneration dentine, t8i. 

Regeneration epithelium, 181. 



398 



INDEX. 



Regeneration mucoid, 179. 
Regeneration muscle, 182. 
Regeneration nerve, 182. 
Regeneration osseous tissue, 180. 
Regeneration white fibrous, 179. 
Regeneration yellow elastic, 180. 
Regenerative inflammation, 175. 
Regenerative power, 177, 
Remittent fever, 342. 
Reinnervation, 182. 
Renal adeno-sarcoma, 328. 
Renal tubular calculi, 233. 
Renal pelvic, 233. 
Resistance to tumors, 273. 
Retention cyst, i^sy. 
Retention theory of immunity, 87. 
Retrogressive tissue changes, 195-6. 
Retrogressive tissue in tumors 274. 
Rhabdomyoma, 297. 
Rhexis, 113. 
Rigor mortis, 264. 
Ringworm, 49. 
Round cell sarcoma, 302. 
Rupture, 40-183. 



Saccharomyces, 51. 
Saccharomyces cerevisiae, 51. 
Saccharomyces farciminosus, 52. 
Salivary calculi, 235. 
Saponification, 258. 
Sarcinae, 53. 
Sarcoma, 298. 
Sarcoma alveolar, 309. 
Sarcoma cells, 300. 
Sarcoma mixed cell, 308. 
Sarcoma mveloid cell, 306. 
Sarcoma round cell, 306. 
Sarcoma structure,, 301. 
Sarco-chondroma, 317. 
Sarco-endothelioma, 312. 
Sarco-fibroma, 3,12. 
Sarco-hemangioma, 318. 
Sarcr'-lymphoma. 303. 
Sarco melanoma, 315. 
Sarco-myxoma, 316. 
Sarco-osteoma, 318. 



Schistosis, 95. 
Schizomycetes, 52, 
Scirrhous carcinoma, 321. 
Sebaceous cyst, ^^7. 
Secondary tumors, 272. 
Senile atrophy, 197. 
Senile necrosis, 258. 
Sequestration, 261. 
Sequestrum, 261. 
Serous exudate, 154. 
Serous inflammation, 220. 
Serous inflammation appearance, 220. 
Serous inflammation cause, 220. 
Serous inflammation effects, 220. 
Siderosis, 248. 

Significance of inflammatory exu- 
date, 156. 
Signs of death, 264. 
Signs of inflammation, 160. 
Situs Viscerum inversus, 102. 
Sodium urate, 223. 
Specific inflammation, 174. 
Specificity law of, 178. 
Spina bifida, 96. 
Spindle cell sarcoma, 325. 
Sporotrichium audouini, 49. 
Sporulation, 56. 
Stadium decrementi, 341. 
Stadium incrementi, 340. 
Staining, post mortem, 264. 
Stearin, 203. 
Sternopagus, 107. 
Sthenic fever, 342. 
Streptococcus, 53. 
Stimulus, 139. 
Stocking, 121. 
Substitution, 185. 
Sub-surface necrosis, 256. 
Suppuration, 167. 
iSuppuration subsurface, 170. 
Suppuration surface, 167. 
Suppurative osteitis, 169. 
Surface necrosis, 156. 
Symmetrical duplicates, 106. 
Synactosis, 95-8. 
Syncope, yy. 
Syncytium, 153. 



INDEX. 



399 



Syncytioma malignum, 33,1. 
Syndactylus, 98. 
Synmelus aprs, 59. 
Synmehis dipus, 98. 
Synmelus monopus, 99. 
Synorchism, 99. 
Synophthalmia, 98. 



Tattooing, 248. 

Temperature, cause of cloudy swell- 
ing, 201. 

Temperature^ cause of degenerations, 
196. 

Telophase, 28. 

Teratoid tumors, 269. 

Teratoma, t,t,2. 

Termination of disease, 75. 

Tests for death. 265. 

Thermic cau.ses of disease, 42. 

Thermic necrosis, 254. 

Tkermogenesis, 340. 

Thermolysis, 340. 

Thoracopagus, 107. 

Thoracoschisis, 97. 

Thrombosis, 122. 

Thrombosis cause, 123. 

Thrombosis, effects, 127, 

Thrombus, 122. 

Thrombus annular, 124. 

Thrombus appearance, 124. 

Thrombus calcification, 127. 

Thrombus complete, 124. 

Thrombus decolorization. 125. 

Thrombus, extension, 124. 

Thrombus infective softening, 126. 

Thrombus location, 12.3. 

Thrombus organization, 126. 

Thrombus parietal, 124. 

Thrombus red, 124. 

"^'^rombrs simple softening, 125. 

"l^rcmbus white, 124. 

'~'"ei tonsurans, 49. 

Tophi, 223. 



Toxic immunity, 84. 

Toxophore, 89-90-91. 

Transportation of visceral organs, 
102. 

Traumatic wounds, 184. 

Tricephalus, 109. 

Tricophyton tonsurans, 49. 

Tubercle, 349. 

Tuberculin, 354. 

Tuberculin test, 354. 

Tuberculosis, 344. 

Tuberculosis extent^ 344. 

Tuberculosis etiology, 345. 

Tuberculosis avenue of infection, 346. 

Tuberculosis source of infection, 346. 

Tuberculosis lesions, 347. 

Tuberculosis extension, 353. 

Tuberculosis elimination, 354. 

Tumors, 267. 

Tumors benign, 277. 

Tumors body resistance, 273. 

Tumors cause, 275,. 

Tumors cells, 269. 

Tumors clinically, 275. 

Tumors color, 271. 

Tumors consistency, 272. 

Tumors extension, 272, 

Tumors frequency, 268, 

Tumors growth, 272. 

Tumors histoid, 277. 

Tumors intercellular substance, 269. 

Tumors malign, 277. 

Tumors metastasis, 272. 

Tumors mottled, 271. 

Tumors number, 272. 

Tumors nutritive supply, 269. 

Tumors organoid, 277. 

Tumors primary, 272. 

Tumors retrogressive changes, 274. 

Tumors secondary, 272. 

Tumors shape, 271. 

Tumors size, 270. 

Tumors structure, 268. 

Tumors teratois,, 277. 

Tumors varieties, 277. 

Twins, 106. 



400 



INDEX. 



u 

Ulcer, 164. 

Ulceration, 164. 

Ulcerative inflammation, 174. 

Union dorsal, 106. 

Union posterior, 106. 

Union ventral, 106. 

Urates, 223. 

Uratic infiltration, 223. 

Uratic infiltration appearance, 223. 

Uratic infiltration cause, 223. 

Uratic infiltration effects, 224. 

Ureter calculi, 234. 

Uretheral calculi, 234. 

Uric acid, 223. 



Venom, 48. 

Vesicle, 42. 

Vesicular inflammation, 174. 

Viper, 48. 

Vitiligo, 250. 

w 

Wandering cells, 152. 

White, fibrous regeneration, 179. 

Wound, 40. 

Wound cause, 184. 

Wound healing, 184-5. 

Wound subsurface, 184. 

Wound surface, 184. 

Wound traumatic, 184. 



Valvular insufficiency, no. 

Valvular stenosis, no. 

Varieties of tumors, 277. 

Vascular buds, 178. 

Vascular constriction, inflammation, 

146. 
Vascular dilation, 147. 
Vascular permeability, in. 
Vascular regeneration, 178. 
Vascular variations, in. 
Vascularization, 178-185. 
Venesection in fatty changes, 205. 



Xanthosis, 245. 
Xiphopagi, 107. 



Yellow elastic regeneration, 184. 



Zooparasites, 63. 
Zootoxins, 78. 



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